Paradoja Osteologica - Wood Et Al 1992

The Osteological Paradox: Problems of Inferring Prehistoric Health from Skeletal Samples
[and Comments and Reply]

Author(s): James W. Wood, George R. Milner, Henry C. Harpending, Kenneth M. Weiss, Mark
N. Cohen, Leslie E. Eisenberg, Dale L. Hutchinson, Rimantas Jankauskas, Gintautas Cesnys,
Gintautas Česnys, M. Anne Katzenberg, John R. Lukacs, Janet W. McGrath, Eric Abella Roth,
Douglas H. Ubelaker and Richard G. Wilkinson
Source: Current Anthropology, Vol. 33, No. 4 (Aug. - Oct., 1992), pp. 343-370
Published by: The University of Chicago Press on behalf of Wenner-Gren Foundation for
Anthropological Research
Stable URL: http://www.jstor.org/stable/2743861 .
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CURRENT ANTHROPOLOGY Volume 33, Number 4, August-October i992
? i992 byThe Wenner-Gren Research.All rightsreservedooII-3204/92-3304-OOOI$2.50
FoundationforAnthropological
i982. He has been curator oftheMuseumofAnthropology ofthe
The Osteological
University ofKentuckyand has conductedarchaeological field-
workin Illinois.He has published"Social and TemporalImplica-
tionsofVariationamongAmericanBottomMississippianCeme-
teries"(AmericanAntiquity49:468-88), "The Late Prehistoric
Paradox CahokiaCulturalSystemoftheMississippiRiverValley:Foun-
dations,Florescence,
history4:I-43),
and Fragmentation"(Journalof WorldPre-
and (withD. H. Humpfand H. C. Harpending)
"PatternMatchingofAge-at-Death Distributionsin Paleodemo-
graphicAnalysis"(AmericanJournal ofPhysicalAnthropology
Problemsof InferringPrehistoric 80:49-5 8).
is Professor
in theDepartmentofAn-
Health fromSkeletal Samples'
HENRY C. HARPENDING
thropology and the GraduateProgramin Geneticsat Pennsylva-
was bornin and nia StateUniversity.He I944 educatedat Ham-
iltonCollege(B.A.,i964) and HarvardUniversity (Ph.D., I972).
He taughtat theUniversity ofNew MexicofromI972 to I985.
by JamesW. Wood, Amonghis publicationsare (withL. Sattenspiel)"StablePopula-
tions and Skeletal Age" (American Antiquity 48:489-98), (with
GeorgeR. Milner, A. Rogersand P. Draper)"Human Sociobiology"(Yearbookof
PhysicalAnthropology 30: I27-50), (withR. Pennington) "Age
HenryC. Harpending, Structure and Sex-biasedMortalityamongHereroPastoralists"
(Human Biology 63:327-52), and (withA. Rogers)"Population
GrowthMakes Wavesin theDistribution ofPairwiseNucleotide
and KennethM. Weiss Differences" (MolecularBiologyand Evolution,in press).
KENNETH M. WEISS iS Professor ofGeneticsand Anthropology at
Pennsylvania StateUniversity. Bornin I94I, he receivedhis B.A.
fromOberlinCollegein I963 and his Ph.D. fromtheUniversity
ofMichiganin I972. He taughtat the CenterforDemographic
Paleodemography and paleopathology presupposethatdirectrela- and PopulationGenetics,GraduateSchoolofBiomedicalSci-
tionshipsexistbetweenstatisticscalculatedfromarchaeological encesand SchoolofPublicHealth,University ofTexas,Houston,
skeletalseries(e.g.,skeletallesionfrequencies and mean age at fromI973 to I984. His publicationsincludeDemographic Mod-
death)and thehealthstatusofthepastpopulationsthatgaverise els forAnthropology (Washington, D.C.: SocietyforAmerican
to theseries.However,threefundamental conceptualproblems Archaeology, I973), (withR. E. Ferrell and C. L. Hanis) "A New
confoundtheinterpretation ofsuch statistics:demographic non- WorldSyndrome ofMetabolicDiseases witha Geneticand Evo-
selectivemortality,
stationarity, and unmeasured, individual- lutionaryBasis" (YearbookofPhysicalAnthropology 27:15 3-78),
levelheterogeneity in therisksofdiseaseand death.Usingsim- "A SurveyofHumanBiodemography" (Journal of Quantitative
ple modelsoftherelationship betweenindividual"frailty" and Anthropology I :79-I 5 I), and The GeneticCauses ofHuman
thehazardofdeathat each age,thispaperexplorestheimplica- Disease (Cambridge:CambridgeUniversity Press,in press).
tionsoftheseproblemsforarchaeologicalinterpretation. One
conclusionis thatthe skeletalevidencepertaining to thetransi- The presentpaperwas submittedin finalform28 XI 9I.
tionfromhunting-and-gathering to settledagricultureis equally
consistentwithan improvement in healthand a deterioration in
healthresulting fromthetransition.
Measurement and interpretationof differencesin the
JAMES W. WOOD ofAnthropology
iS AssociateProfessor and Se- level ofhealthin prehistoricpopulationsare two funda-
niorResearchAssociateofthe PopulationIssues ResearchCenter mental goals of paleodemographyand paleopathology.
at Pennsylvania StateUniversity (University Park,Pa. i6802, Studiesofsuch differences arevital to ourunderstanding
U.S.A.).Bornin I949, he was educatedat ColumbiaUniversity of how the adaptive success of human populationshas
(B.A.,I97I) and theUniversity ofMichigan(M.A.,I975; Ph.D.,
variedthroughtime and space. Forthe purposesofthese
ig80). He has taughtat Michiganand at theUniversity ofWis-
consinand has donefieldwork in demography, reproductive biol- studies,several standardindices of morbidityand mor-
ogy,and populationgeneticsin Papua New Guinea.His publica- talityderivedfromskeletal series (e.g., skeletal lesion
tionsinclude"Fertilityin Anthropological Populations"(Annual frequencies,life expectancies,and averageage at death)
ReviewofAnthropology i9), "Fertilityand Reproductive Biology would seem readilyinterpretable.Common sense sug-
in Papua New Guinea,"in Human Biologyin Papua New
Guinea,editedby R. D. Attenborough and M. P. Alpers(Oxford: geststhatthereshould be some reasonablydirectassoci-
OxfordUniversity Press,i992), and DynamicsofHuman Repro- ation between these aggregate-levelmeasures and the
duction(Hawthorne:Aldine,in press). risksof illness and death experiencedby the individual
GEORGE R. MILNER is AssociateProfessor and MuseumCurator membersof past populations.For example, an increase
in theDepartmentofAnthropology at Pennsylvania StateUni- in the frequencyof a particulartype of skeletal lesion
versity.He was bornin I953 and receivedhis B.A. fromBeloit mightbe interpretedas indicatingan elevation in the
Collegein I975 and his Ph.D. fromNorthwestern University in
individualrisks of experiencingthe conditionsthat in-
duce the lesion and hence an increasein the population
i. A versionof thispaperwas presentedat the I989 meetingsof prevalenceof those conditions.Similarly,a decrease in
the SocietyforAmericanArchaeology in Atlanta,Ga. We thank the average age at death might be taken as signaling
Eve Anderson,Gillian Bentley,Anne Buchanan,TimothyGage, an elevation in the risks of death experiencedby the
DarrylHolman,PatriciaJohnson, Paul Leslie,ClaireMcHale Mil-
ner,and RichardPaine forcommentsand suggestions.We also individualsin the once-livingpopulation.Most interpre-
thankthe Illinois State Museum forpermissionto examinethe tationsof paleodemographicand paleopathologicaldata
Oneotaskeletalcollection. presupposethatsuch straightforward relationshipsexist.
343

344 CURRENT ANTHROPOLOGY Volume 33, Number 4, August-October 1992
We suggestthatinterpretation of these standardmea- summarystatisticssuch as lifeexpectanciesor themean

sures may be more difficultthan it firstappears,espe- age at death are ofteneffectivelymeasures of fertility
cially when dealing with skeletonsfromarchaeological ratherthan mortality.
contexts.Failure to addressthreeimportantconceptual The implications of this basic fact of mathematical
issues-demographic nonstationarity, selectivemortal- demographyforprehistoricskeletal samples have been
ity, and hidden heterogeneityin risks-can renderin- discussed elsewhere (Sattenspieland Harpendingi983,
ferencesbased on various demographicand epidemio- Johannsonand Horowitz i986, Milner,Humpf,and Har-
logical measures meaningless.These problemsare, we pending i989, Paine i989). Paleodemographershave
believe,amongthe most difficultcurrently facingrecon- startedto pay some attentionto this problem,although
structionsof the demographyand healthofpast popula- theystill tendto underrateits importance(Cohen i989).
tions, far more difficultthan the issues raised by Because the issue of demographicnonstationarity is not
Bocquet-Appeland Masset (i982) in their"Farewell to new,we concentratein thispaperon the othertwo prob-
Paleodemography"(indeed, their points have largely lems, selective mortalityand hidden heterogeneityin
been addressedbyVan Gervenand Armelagos[i 9831and risks. This treatmentis convenientbecause those two
Buikstraand Konigsberg[i985], among others). problemsare fundamentallyrelated: in the absence of
This paperis not,however,a counsel ofdespair.Con- heterogeneity, selectivitydoes not occur.
tinualreexaminationofunderlyingpremisesis essential The selective mortalityproblemis easy to state but
to any vigorousfield of research.In the case of paleo- difficultto solve. There is one, and perhaps only one,
pathology,studies of ancient bone have undergonesig- irrefutable factabout the cases makingup a skeletal se-
nificantchangesin orientationand sophisticationsince ries: they are dead. We never have a sample of all the
the mid-ig6os (Armelagos,Goodman, and JacobsI978, individuals who were at risk of disease or death at a
Buikstraand Cook I980, Huss-Ashmore,Goodman,and given age, but only of those who did in factdie at that
Armelagos i982, Ubelakeri982, Martin, Goodman,and age. For example,the only 2o-year-oldswe observein a
ArmelagosI985, LarsenI987, Ortnerand Aufderheideskeletal sample are those who died at age 2o. While we
I99I). During this period,the field has moved froma may findthe skeletonsofmany of the otherindividuals
particularisticconcernwith individuallesions or skele- who had been at risk of death at age 2o but who died
tons to a population-basedperspectiveon disease pro- later,say, at age 6o, we observetheircharacteristicsas
cesses, the evolution of humans and their pathogens, 6o-year-olds, not 2o-year-olds.As a result,the sample of
and the evaluationofpast communityhealth,especially 2o-year-olds(or any otherage-group)is highlyselective
as it has changed with the adoption of fundamentally forlesions that increase the risk of death at that age.2
new ways oflife.Similarly,paleodemography has moved Estimatesof the populationprevalencesof such lesions
fromsimple and oftenidiosyncratictabulationsof age fromskeletalseriesare therefore subjectto preciselythe
and sex data to more rigorousanalyticalinvestigations same sortof selectivitybias as the derivationofpopula-
of demographicprocesses in prehistoricpopulations tionprevalencesfromclinical data,because neithertype
(Angeli969, Acsadi and Nemeskeri I970, Weiss I973, of data constitutesa representativesample of the entire
UbelakerI974, Moore,Swedlund,andArmelagosI975, populationat risk.In both cases, the observedfrequency
BuikstraI976, Lovejoyet al. I977, Lallo, Rose, and Arm- of pathologicalconditionsshould overestimatethe true
elagosI980, Buikstra andKonigsberg I985, Buikstra and prevalenceof the conditionsin the generalpopulation.3
Mielke I985, Buikstra,Konigsberg,and BullingtonI986, This bias cannot be avoided simplyby obtaininglarger,
Johannsonand Horowitz i986, Horowitz, Armelagos, morerepresentative skeletal samples; it is builtinto the
and Wachter I988). The concerns raised in this paper verystructureof the data.
would not be relevanthad paleopathologyand paleode- The problemof hidden heterogeneityin risks is per-
mographynot become established fields of active re- haps more counterintuitive. In the presentcontext,hid-
search. den heterogeneitymeans that the population from
2. Thisselectivity
differsfromthatattributable tohavingan unrep-
Conceptual Problems resentativesampleofthedead,forexample,becauseofpoorpreser-
vationofinfantskeletons.Ourpointis thatall samplesofthedead
areinherently unrepresentative oftheoriginallivingpopulationat
Demographicnonstationarityrefersto the departureof riskof death,even a skeletalcollectionthatis a perfectrandom
a populationfromthe stationarystate-a state charac- sampleofall thosewho died.
terizedbyclosureto migration,constantage-specificfer- 3. This generalization
leaves aside thequestionofhow sensitivea
tilityand mortality,zero growthrate, and an equilib- skeletallesion may be as an indicatorof disease. Pathological
rium age distribution.In nonstationarypopulations, changesin bone tend to be markersof chronicconditions,and
oftenonlya smallfraction ofcases developsskeletallesions.Thus,
age-at-deathdistributionsare extremelysensitive to as paleopathologists
frequently pointout,skeletallesionsmaybe
changes in fertilitybut not to changes in mortality expectedto underestimate thepopulationprevalencesoftheiras-
(Coale I957, Keyfitzi985). Thus,ifa population is not sociatedconditions.Atpresent,it is difficult
to weighthecounter-
stationary-and changingpopulationsneverare-small vailingeffects
oftheunderestimation causedbylow sensitivity and
theoverestimation causedbyselectivity bias.Thereis no reasonto
variationsin fertilityhave large effectson its age-at- expect,however,thattheseerrors willperfectlybalanceeachother.
deathdistribution,while even quite largemodifications Therefore,we doubtthatitwilleverbe possibletoestimatepopula-
of mortalityhave virtuallynone. Paradoxically,then, tiorn nrPr7,nlPnrcPQrplinbhlIT frl-n qrkPl.tnl Lgiryn fIrP.a11PnC

WOOD ET AL. The Osteological Paradox | 345
which the skeletal series is drawn was made up of an disease and typicallybeforea bonyresponseis elicited;
unknownmixtureofindividualswho variedin theirun- in this group,rapiddeath resultsin few,if any,skeletal
derlyingfrailtyor susceptibilityto disease and death.4 lesions in the mortalitysample. Consideringthe differ-
Such heterogeneity may arise fromgeneticcauses, from ential exposure to stress experienced by these three
socioeconomic differentials, frommicroenvironmental groups,it seems appropriateto rank them fromhigh to
variation,or even fromtemporaltrendsin health,since low accordingto theirlevel of health,at least with re-
most skeletal series,especially largeones, representac- spect to the condition of interest.Judgingsolely from
cumulations over more or less prolonged periods of the skeletal lesions, however, there appear to be not
-time.Hidden heterogeneityin risks makes it virtually threegroupsbut onlytwo: one healthy(unstressed)sub-
impossibleto interpretaggregate-level age-specificmor- populationwith no lesions and one stressedsubpopula-
talityrates in terms of individual risks of death. This tion with many. The groupsexperiencingthe least and
problemis farfromrestrictedto archaeologicalsamples themost stressare indistinguishablewithrespectto the
but is now widely acknowledgedthroughoutdemogra- distributionof this particularkind of lesion.
phy (Vaupel and Yashin i985a, b; Trussell and Rodri- This fictitious(but not implausible) example intro-
guezI990). duces several of the themes exploredin this paper: the
All these problems reflect two unavoidable facts. possible presence within the population of interestof
First,it is impossibleto obtaindirectestimatesofdemo- multiple,undetectedsubgroupsthat experiencevarying
graphic or epidemiological rates from archaeological risks of disease and death, the difficultyof recon-
samples. Such estimates require that we know the structingpopulationprevalencesof pathologicalcondi-
amount of exposureto the risk of illness or death,that tionsfromskeletallesion frequencies,the complexrela-
is, thenumberofindividualsexposedto the riskand the tionshipbetweenthe degreeof stressand the likelihood
length of their exposures, neither of which is ever ofdevelopinga lesion, and the possibilitythatindividu-
known with sufficientprecision in archaeological re- als displayinglesions may actuallybe healthierthan at
search to permitformalestimationby standardmeth- least some individualswithoutlesions. In what follows,
ods. Assumptions such as stationarityare ruses that we show how each of these factorscan confoundthe
allow us to reconstructexposure indirectly,if imper- interpretation of osteological evidence about the health
fectly.Second, although "health" (howeverdefined)is of past populations.
a biological characteristicof the individual,inferences
about it must be based on aggregate-or population-level
statistics.Justas it is a truismin epidemiologythat the Hidden Heterogeneityand the Deviant
single-casestudyis of limitedvalue, it is widelyrecog- Dynamics of Death
nized in paleopathologythatreportson singlespecimens
tell us littleabout the disease experienceofancientpop- Life-tableestimates of age-specificmortalityare often
ulations. However, when the population of interestis used in paleodemographyto draw inferencesabout the
heterogeneousforfactorsthataffecthealth,therelation- levels and age patternsofrisksexperiencedbyindividual
ship between aggregatemeasures and the experienceof members of the population being studied. However,
the individualsmakingup the aggregatecan be remark- when individualsvary in frailtyand thus theirrisk of
ably tenuous. death and this variationis "hidden" (i.e., not captured
For example,imagine a livingpopulation comprising by observed covariates), death rates computed from
three subpopulations,all of which are potentiallyex- aggregate-level mortalitydata may providea misleading
posed to an acquired conditionreflectingsome formof pictureofindividual-levelrisks.This can be shownwith
stress.This condition,when it occurs,increasesthe risk a verysimple model, one thatis intendednot to be par-
ofdeathand may eventuallyproducea distinctiveskele- ticularlyrealisticbut simplyto make a basic pointabout
tal lesion in survivors.Members of the firstsubpopula- hidden heterogeneityand what Vaupel and Yashin
tionneverexperiencethe stress;therefore, none ofthem (i985b) call "the deviantdynamicsof death."
developsskeletal lesions. The second subpopulationex- Imagine that we observe a population of newborns,
periences moderate stress, sufficientto cause wide- each of whom experiencesan absolutelyconstantrisk
spreadsickness lastinglong enoughto producebonyle- of death but who varyamong themselvesin theirrisks.
sions but causing few deaths; most individuals with The hazard of death (the continuous-timeanalog ofthe
bony lesions survive the stress but join the mortality centralmortalityrate in the life table) experiencedby
sample later when they succumb to some other cause each child mightbe modeled as h,(t) = zi hc, where t
of death. The thirdsubpopulationsuffersheavy stress, is the child's age, zi is a measure of its individual-level
resultingin numerousdeaths soon afterthe onset ofthe frailty,and h, is a componentof the hazard common to
all childrenin the population.While we writehi(t) as a
4. The termfrailty,whichhas enteredstandarddemographic usage, functionof age, both zi and h, are constants;therefore,
was originallydefinedby Vaupel,Manton,and Stallard(I979) as the overall hazard for the ith child does not in fact
an individual'srelativeriskof deathcomparedto a standardized changewith age.
cohortrisk.Moregenerally, itrefers
toindividualbiologicalcharac-
teristicsassociatedwithpersistentdifferencesamongindividuals Now suppose that z1 is distributedin some regular
in susceptibility, orrelativeriskwithrespectto disease
propensity, fashionamong the newborns;forexample,the frailtyof
or death(Vaupeli990). newbornsmightbe normallydistributedas in figurei,

60
go(z)
<},> 50 _
WEEK 0 40
:5 30 \
ZO 20 -
10
0
0 1 2 3 4 5
~~~~~~~~ 0
Age of child(years)
zo z
0.25
- 020
~020 A
\h(t) = 0.244exp[-0.751(t)1
c 015 r2 0.901 (onlogscale)
* 001
.10\
*Q
4-
000
o.o
0 1 2 3 4 5
Ag9ofchtk(years)
FIG. 2. Observed age-at-deathdistributionup to age
fiveyearsfroma late prehistoric(A.D. I300) Oneota
site in west-centralIllinois (Milnerand Smith I990)
FIG. I. A model ofheterogeneousfrailtyand selective and (below) age-specifichazards of death estimated
mortality.Each child's hazard of death is assumed to fromthe age-at-deathdistributionunder the
be constantand proportionalto its individual-level assumptionthat the Oneota population was
frailty(z). Frailtyin turnis assumed to be normally stationary.The smooth curveis a two-parameter
distributedamong newborns (top).Deaths duringthe negative Gompertzfunctionfittedto the hazards by
firstweek oflife (dots)are selective withrespectto ordinaryleast squares.
thefrailtydistribution;that is, childrenofhighfrailty
make up a disproportionately large fractionof all
deaths. As a consequence, the frailtydistribution are selectivewith respectto the frailtydistribution:the
shiftsdownward by the second week oflife (bottom), greatera child's frailty,
the morelikelyit is to die. Thus,
and mean frailtydecreases (arrow).Since the the frailtydistributionshiftswith age as high-frailty in-
aggregate-level hazard of death at each age is dividuals are eliminatedby death (fig.i, bottom).As a
proportionalto the mean frailtyof survivorsat that result,the mean frailtyof survivingchildrendeclines
age, the aggregatehazard declines even thoughthe with age, causing the mean hazard of death to decline
hazards of the individual childrenremain constant. as well. In otherwords,the aggregate-level riskofdeath,
givenby the mean hazard, dropswith age even though
top.Ifgt(z)is the probabilitydensityfunctionspecifying the individual-levelrisks remain absolutely constant.
that distributionat age t, then the mean hazard forall Thus, wherethereis heterogeneity in frailty,changesin
the childrenalive at age t is the aggregate-levelhazard do not reflecttherisksexperi-
enced by any of the individualswho make up the popu-
h(t) =f gt(z)zhcdz= Zh (I )
lation.
The confoundingeffectthatheterogeneousfrailtycan
have on the relationshipbetween aggregate-levelmor-
In otherwords,the mean hazard at any givenage is sim- talityand individualhealthcan be illustratedwithrefer-
ply the productof the common hazard and the mean of ence to a real archaeologicalsample. Figure2, top,shows
the frailtydistributionat that age. the age-at-deathdistributionup to age fiveyearsforan
The crucial point here is thatbothgt(z)and Z-tchange unusuallywell-preserved sample oflate prehistoricskel-
over time, because deaths of childrenat any given age etons froma completelyexcavated Oneota,cemeteryin

west-centralIllinois (Milnerand Smith i990). A total of Unfortunately,the aggregate-levelhazards of death

264 skeletonsis includedin thissample,withI25.4 of may tell us disturbinglylittle about individualrisks of
them estimatedto be below age five.5The age-at-death disease and death if the population is heterogeneous
distributionclosely approximatesthe mortalitypatterns with respect to frailty,as any real population almost
expectedof a traditional,preindustrialpopulationwith certainlymust be. For example,assume thatthe Oneota
high fertility(Milner, Humpf, and Harpending I989, populationthatgave rise to the skeletal sample was ac-
Paine i989). Most important,thereis no obvious under- tuallymade up of two distinctand nonoverlappingsub-
enumerationof the veryyoung in this sample, a com- populations,denoted i and 2, with differing levels and
mon problem in archaeological collections. The age- age patternsof mortality.Of course, there is no prior
specifichazards of death estimatedfromthis sample by reasonto believe that exactlytwo subpopulationsexist,
standardlife-tabletechniques6are entirelyplausible for but this is the simplest formof heterogeneityimagin-
this sort of population (fig.2, bottom),with mortality able. For furthersimplicity,assume that each subpopu-
duringthe firstsix months of life just above 2oo per lation was homogeneouswith respectto death (i.e., ev-
i,ooo live birthsand a rapid and consistentdecline in eryindividualwithina givensubpopulationexperienced
mortalitybeyond early childhood. The estimatedrates the same hazard of death at each age). How mightthe
are fitquite satisfactorily by a two-parameter Gompertz two subpopulationsbe combinedto yield the Gompertz
hazardfunction(fig.2, bottom),a model that is widely mortalitycurve characteristicof the Oneota skeletal
used to describethe decline in human mortalityat early sample as a whole?
ages (Gage I990).7 From this point on, we will take the The model presentedin the appendixprovidesa way
fittedGompertzcurve as a reasonablerepresentationof to address this question. All that has to be done is to
earlychildhoodmortalityin the Oneota population,as specifya mathematicalformforthe age-specifichazard
estimatedat the aggregatelevel. functionin one of the subpopulationsin orderto find
What do these aggregatemortalityrates reveal about the correspondingfunctionin the other. Suppose, for
therisksofmorbidityand mortalityexperiencedbyindi- example, that the population contains a groupof rela-
vidual childrenin the Oneota population? A conven- tivelydisadvantaged(i.e., frail)childrenwho represent
tional interpretation, common in both the health sci- approximatelyhalf of all newborns. If the hazard of
ences and paleodemography,is that the "average" death forthese childrenis constantand equals o.25 at
newborninfantis at a high risk of death but its risk all ages, then we have the mixtureof subpopulations
declines rapidlyas it grows older. This interpretation, shown in figure3, A. The hazard experiencedby the
which would arouse no controversy, is not necessarily second, less frail subpopulationnow declines at early
consistentwithrecentindividual-levelstudiesofdisease ages, but it does so much more rapidlythan the aggre-
processesand specificcauses of death.For example,the gate mortalitycurve,reachingzero by about one yearof
risksof morbidityand mortalityfromdiarrhealdisease, age. In this instance,the aggregatehazard curve is not
a major killer of children in the contemporaryThird an accuratereflectionof the hazards experiencedby in-
World,tend to increase over the firstseveralmonthsof dividualsin eithersubpopulation.Instead,the shape of
lifeas exposureto pathogensincreasesand as maternal the aggregatehazard functionis dominatedby a selec-
antibodiesfrombreastmilkdecline (Long et al. i992). tionprocess:because oftheirhighriskofdeath,children
And yet the hazard rates in figure2 seem to speak for in subpopulationi are progressivelyselected out of the
themselves:the risk of death is initiallyhigh but then initial pool of newborns,and subpopulation2 comes to
declines steadily. representan ever-increasingfractionof all surviving
children.The aggregatehazard thus convergeson the
5. Fractionalindividualsresultfromthe way in whichskeletons hazard of subpopulation2 as time goes by.
assignedto variousages are distributed overadjacentsix-month Next, suppose that the hazard in subpopulationi re-
intervals,a reflectionofuncertainty in estimating theage ofindi-
viduals.
mains constantwith age but dropsto o. i 6 and that the
6. These hazardrateswereestimatedon the assumptionthatthe fraction ofnewbornsbelongingto subpopulationi is re-
populationwas stationary(see Milner,Humpf,and Harpending duced to 0.4. These changesproduce the curves shown
I989, Paine i989). We makethisassumption forcon- in figure3, B. Now the hazardfunctionin subpopulation
herestrictly
venience,sinceourintentionis notto highlight thenonstationar- 2 startsout higherthan the aggregatecurve but drops
ityproblembutratherto focuson theissues ofheterogeneity and
selectivity.Paine (i989) appliedmaximum-likelihood methodsto below it at about nine monthsof age. Again,the aggre-
fitmodelstablepopulationsto the Oneota sampleand estimated gate hazards fail to capture the patternof risks of any
that the population growthrate was approximately -0.002. This individualsin the population.
estimatesuggeststhat,whiletheOneotapopulationmaynothave An immediatereactionto these subpopulationhazard
been absolutelystationary, it was probablynot farfromit. How-
ever,becausethe likelihoodsurfacewas quiteflatnearthemaxi-
curves is liable to be that,while mathematicallypossi-
mum,it is impossibleto ruleouteitherpositiveornegativegrowth ble, theymake littlesense fromeithera demographicor
ratesofsmall absolutevalue. Consequently, thehazardsin figure a biologicalpoint ofview. We suggestthatthis reaction
2 shouldnotbe takenas finalestimatesofmortality at theseages. may be incorrect,preciselybecause commonsense no-
7. ManyapplicationsoftheGompertzfunction to preadultmortal- tions about what age-specificmortalityrates ought to
ity use a three-parameter formthat includes a constant,age-
independent component(we aregrateful to TimothyGageforthis look like are based entirelyon aggregate-level data. By
observation).Fortheage-range consideredhere,thismorecompli- and large,we have littleidea how hazardsshouldbehave
catedspecification addslittleto the analysis. at the individuallevel. As we have alreadynoted,there

0.32 I I I 0.32
A B
hl(t)
0.24 024
N hl~~~~~~~~~~~~~~~~~~~~~(t)
0.08 0.08
0.12 C 0.321, I , W
0.00 0.00
0 1 2 3 4 5 0 1 2 3 4 5
0.32 0.32
C D
0m24 4hat
mixture assuming that h04h=(t)
the
= 0.16
0.0
r-4
0.16 hi(t) ~~~~~~~~~~0.08
2 2~~~~~~~~~~~~~~~~~~~~~
0.00 .0
0.00
~~~~~~~~~000
0 1 2 3 4 5 0 1 2 3 4 5
Ageofchikld
(years) Ageofchild(years)
mixturesof subpopulationhazards, hl(t) and h2(t),all of which are equally consistentwith the
FiG. 3. Different
same Gompertzfunctionforthe average age-specifichazard, h(t) (based on the two-pointfrailtymodel of
Vaupel and Yashin [i985a]). In each case, the Gompertzcurveis the same as in figure2 (bottom).A, the
mixtureassuming that hl(t) = 0.25 and p (theproportionofnewbornsbelongingto subpopulation i) = 0.5; B,
the mixtureassuming that hl(t) = o.i6 and p = 0.4; C, the mixtureassuming that hl(t) = 0.02 + 0.04t and p
= 0.4; D, the mixtureassuming that hl(t) =0.3 - o.it and p = 0.2.
is reason to suspect that the hazard for diarrheamay a given aggregatemortalitypatterncan result froman
actuallygo up at earlyages as the durationof exposure infinitenumberof possible combinationsof subpopula-
increases,and the same is likelyto be trueofotherinfec- tion mortalities.Moreover,we rarelyif ever have any
tious diseases. Figure3, C, allows forsuch an increasing idea how many subpopulationsactually exist. It could
hazard in subpopulationi. Althoughradicallydifferent in factbe two, but it could also be three,four,or more,
fromthe aggregatepattern,an increasinghazard in one and indeed at the limit everyindividualcould have his
subpopulationis perfectlycompatiblewith a decreasing orherown unique level offrailty, givingrise to the sorts
aggregatehazard so long as the hazard in subpopulation of continuousdistributionsof frailtyshown in figurei.
2 startshigherthan the aggregatecurvebut dropsbelow This factonly adds to the rangeof possible models that
it at about one and a halfyearsof age. are perfectlyconsistentwith a givenaggregatemortality
Finally,with a lineardecline in thehazardforsubpop- curve.The problemis not simplya reflectionofthe fact
ulation i (fig.3, D), the curve in subpopulation2 be- thatwe have arbitrarily assumed two subpopulations.
haves veryoddly indeed. It roughlyparallels the aggre- This is a specificinstanceofwhat is knownin mathe-
gate hazard up to age two but then skyrocketsas the matical statisticsas the identificationproblem (Hsiao
aggregatecurve approacheszero. I990, LancasterI990). A modelis said to be uniquely
These examples could be multipliedendlessly.How- identifiableif,when fittedto a particularset of data by
ever,the generalpoint of the exerciseshould be clear. If some formal method such as maximum likelihood,
thereis hiddenheterogeneityin the risk of death,then thereis one and only one value of each ofits parameters

that is consistentwith the data. The models we have ples are by definitioncomposed of a veryspecial subset
just reviewedare unidentifiablein thatan infinitenum- of individualswho were exposed to the risk of death at
ber of values of the subpopulationhazards are equally each age,namely,the nonsurvivors.By theirnature,the
compatible with the observed aggregatehazards. Far dead are a biased sample of all the individuals in the
more disturbing,every other model of heterogeneous populationwho were alive at a givenage. Because ofthis
frailty,whetherdiscrete or continuous,is equally un- selectivity,it is surprisingly difficultto drawinferences
identifiable.What this means in practiceis thatthereis about the prevalenceofpathologicalconditionsmarked
no way to inferindividualrisks of death fromaggregate byhard-tissueabnormalitiesin a once-livingpopulation
mortalitydata in the absence of priortheorythat speci- fromthe frequencyof lesions in a skeletal sample. The
fiesthe way in which frailtyvaries among individuals. reason forthis difficulty is simple: if the disease state
The implicationsofthis problemforthe demographic of interestaffectedindividuals' risks of death (and pre-
treatmentofmortalityare profound.Indeed,hiddenhet- sumably that is preciselywhy it is interesting),then
erogeneityin risks and the identificationproblemasso- the frequencyof the disease must be greateramong
ciated with it have become dominant concerns in de- nonsurvivorsthan among the living.Stated differently,
mographyduringthe past decade (Keyfitzand Littman proportionalmortality(the fractionof deaths attribut-
I980; Heckmanand Singeri984b; Vaupeland Yashin able to a particular cause) overestimatespopulation
I985a, b; Heckman and Walker I987; Manton and Stal- prevalencebecause mortalityitselfis selective.
lardI988; LancasterI990; TrussellandRodriguez
I990). Selective mortalityis a special concern when bone
Two generalstrategieshave been developedfordealing lesions thatwere active at the time ofdeath indicatean
withhiddenheterogeneity. One is to model the distribu- elevatedrisk of death. Enhancedrisk may arise directly
tion of frailtydirectlyin a way that makes biological from the disease process that induced the bony re-
sense (Weissi990). Often,however,thereis too little sponse-that is, that particulardisease may be the pri-
priortheoryabout how the relevantprocesses work to marycause of death. Alternatively,the disease may be
permitthis sort of etiologic modeling.The second ap- a contributory cause, orit may simplybe correlatedwith
proachinvolves the developmentof more generalmod- some otherfactorthat affectsmortality.In all these in-
els of heterogeneousfrailty(e.g., Heckman and Singer stances,the presenceof an active skeletal lesion marks
I984a, Trussell and Richards I985, Heckman and a person at elevated risk of death. Therefore,the fre-
WalkerI987, VaupelI990). Hereone specifiesan arbi- quency of active lesions in a skeletal sample is greater
traryprobabilitydensity functionfor the unobserved than the fractionof affectedindividuals in the living
heterogeneity and thenchecks to see ifthe finalnumeri- populationfromwhich the sample was drawn.This is
cal results are robust for changes in the specification. truenot only of the skeletal sample as a whole but also
While it is not yet certainhow successfulthese strate- of its constituentage- and sex-groupsconsideredindi-
gies will be, recentapplicationsin the analysis of data vidually.Withoutknowledgeof the riskofdeath associ-
on morbidityand mortalityoffersome hope (Manton ated with a particularcondition,it is impossibleto pre-
andStallardI988, WeissI990). dict from modern population prevalences (e.g., from
Forthepresent,it is importantforpaleodemographers epidemiological studies) the proportionof a skeletal
and paleopathologiststo be aware of the generalprob- sample that would be expected to show a hard-tissue
lem. When hidden heterogeneityin risks exists, as we response. Despite this fact,direct extrapolationsfrom
suspectit must in all populations,thenpopulation-level clinical and epidemiologicalfindingsto mortalitysam-
mortalitypatternsmay tell us little if anythingabout ples are sometimes encounteredin the literatureon
individualrisks of death. As a consequence, inferences archaeological skeletons (Morse I978, Blakely and
frompaleodemographiclife tables to the health status Detweiler-BlakelyI989).
of individualsin prehistoricpopulations are, to say the The effectsof selective mortalitycan be illustrated
least,problematic.Even ifthe osteologistwishes merely with referenceto the Oneota skeletal series.Numerous
to rankprehistoricpopulationsby theirgenerallevel of crania in this collection exhibit the distinctiveorbital
health,the problemis still important:populationscan- and cranial-vaultlesions usually referredto, respec-
not be comparedmeaningfullyif theirdistributionsof tively,as cribraorbitaliaand porotichyperostosis.These
frailtydifferin unknownways. A solution to this prob- lesions are known to accompanyvarious anemias and,
lem will requireserious thoughtabout the best ways to when encounteredin pre-Columbianskeletonsfromthe
model the variationin frailtythat almost certainlyex- Americas,are usually attributedto iron-deficiency ane-
ists in all archaeologicalcontexts. mia (El-Najjar et al. I976; Steinbock I976; Mensforth
et al. I978; OrtnerandPutscharI985; Stuart-Macadam
I985, I989; LarsenI987; Palkovichi987).8 Thepresence
Selective Mortalityand the Mysterious
Meaning of Morbidity 8. Deficienciesofspecificnutrients
arefrequently
partofa broader
patternofnutritional inadequacy,oftencomplicatedbyinfection.
Heterogeneityand selectivitycomplicatethe interpreta- It has long been arguedthatthe elevatedmortalityratesamong
youngchildrencommonin the contemporary ThirdWorldreflect
tion of morbidityas well as mortality.As has been the interactionof infectionand malnutrition (Gordon,Chitkara,
pointedout (CookandBuikstraI979; Cook 1981, 1984; andWyonI963, Gordon,Wyon,andAscoli I967, Scrimshaw, Tay-
Palkovich1985; Milnerand Smith1990), skeletalsam- lor,and GordonI968, Pufferand SerranoI973, ScrimshawI977,

350 CURRENT ANTHROPOLOGY Volume 33, Number 4, August-October I992
80 -
10
60 - 08 _
~4040
o~~~
0~ ~ 06
(D3
D 06 - \eletal
-0
E
D
z
0
04 reconstructed
o 400 _
20 NONE
_8 Ppopatmn
ACTIVE
[ INACTIVE
02
0.5-4 5-9 10-1415-19 20+
00~~~~~~~~~~-
Age group(years) 00 L I I
FIG. 4. Numbers of Oneota crania in fiveage-groups 0 5 10 15 20

withactive cribraorbitalia or porotichyperostosis,
inactive (remodeled)lesions, and no lesions. While
the differentiation of active and inactive lesions is Age (years)
inexact,it is the overall age pattern,not individual Age-specificproportionsof Oneota crania with
FIG. 5.
crania, that is importanthere. cribraorbitalia or porotichyperostosis(solid curve)
and a reconstructionof the age-specificprevalences of
thoselesions in the livingpopulation (brokencurve).
of these cranial lesions is thoughtto reflecta bony re- Because of the selective effectsofmortality,lesion
sponse in early childhood to pathological expansion frequenciesare higheramong those who died (the
of hematopoietic tissue in restricteddiploic spaces skeletal sample) than in the reconstructedpopulation
(Stuart-MacadamI985). Although iron-deficiency ane- at risk.
mia cetainlyoccurs in laterlifeas well, it is unlikelyto
induce comparablebony responsesat those ages. Once active at the time of death,should be higherthan their
developed, however, these cranial lesions can be re- prevalencein a comparableage-groupin thelivingpopu-
tained throughoutlife,as is indicatedby theirfrequent lation. This is shown in figure5, which presentsesti-
occurrencein the skeletons of adults frommany parts mates of the proportionof the once-livingpopulation
of the world. at each age that may have exhibitedbony lesions. The
In the Oneota skeletal collection,bothcribraorbitalia reconstructed populationat riskat each age was derived
and porotichyperostosisare presenton most ofthejuve- by summingall observedcrania and then decrementing
nile crania but few adult crania (fig.4). Lesions indica- the sum by the numberof individualsthat died in the
tiveofan activebonyresponseare restrictedto children, previousage-group;the numberof individualswith le-
principallythose less than five years old. The discrep- sions at each age in the reconstructedpopulation was
ancyin thenumbersofaffectedjuvenileand adult crania similarly estimated. This reconstructionis based on
presumablyreflectsongoing selectivitythat preferen- threeassumptions:(i) the populationwas stationary,(2)
tiallyeliminatesthe most frailindividualswithin each thebonylesions indicatea conditionthatdevelopeddur-
age interval.The remodeled lesions, in this view, iden- ing the firstfive years of life, and (3) the lesions are
tifyindividualswho managedto survivea periodofearly not entirelyobliteratedby subsequentbone remodeling.
illness only to succumb somewhatlaterto stressof un- Undoubtedly,all these assumptions oversimplifyreal-
knownorigin-stress thatmay or maynot have had any ity.9Nonetheless, they permit a tentativereconstruc-
relationto the conditionsthatproducedthe lesion.
Since we are viewingthe end resultof selectiveentry 9. The assumptionof stationarity has been discussedin n. 6. As-
into the mortalitysample,the frequencyofpathological sumption2 reflects theknownchildhoodassociationofthesebony
hard-tissuelesions, especially those that appear to be responses(Stuart-Macadam i985). Assumption 3 is morequestion-
able,butlesion obliterationthroughprogressive bone remodeling
wouldbe expectedto have its greatesteffectin theadultcategory
Chandraand ChandraI986), and severalosteologistshavestressed (20 yearsand older).If accountcould be taken of this effect,
it
thissynergismin theetiologyofcribraorbitaliaandporotichyper- wouldincreasethereconstructed populationprevalencesbya con-
ostosis (Mensforthet al. I978, Walker I985, Palkovich I987, stantof proportionalitybut not enoughto bringthemup to the
Stuart-Macadam I989). oflesionsin theskeletalsample.
frequencies

WOOD ET AL. The Osteological Paradox I 35I
tion of the population at risk and the frequencyof le- 100

sionsin thatpopulationand therebyrevealtrendsduring
thejuvenileyearsthatreflectselectivemortalityUnder CD
this patternof selectivityacting upon heterogeneous DO 80
susceptibilityto stress,thelesion frequenciesamongthe
dead are consistentlygreaterthan the prevalenceof le- g 60
sions in the livingpopulation. Cu
CO,
It is importantto emphasize that this particularre- co

constructionis based on a series of assumptions (e.g., 40
stationarity)that may not be correct.When such as-
sumptionscannot be made, there is no way to recon-
structthe numbers of individuals at risk and thus no L_ %~~~~~~~~~~~~~
way to inferpopulation prevalences from proportional 20
mortality.
Selective mortalityis also a concernin dealing with 60 80 100 120 140
more subtle markersof poor health. For example, be-
cause ofits known multifactorialetiology,shortstature
Stature(cm)
is oftentakenas an indicatorofgeneralstress.A number
ofresearchershave used the lengthoflongbones in juve- FIG. 6. Effects of two different levels of mortalityon
niles to identifydifferencesin linear growth among the stature of the dead when the risk of death is
groupsof skeletons drawn fromseparate time periods negativelycorrelatedwith staturein the living. Solid
and have linked the bone lengthdata to otherskeletal curve,distributionof staturein the livingpopulation,
evidenceof ill health (Hummertand Van Gerven I983, assumed to be normal with a mean of IOO cm and a
Cook I984, Goodmanet al. I984, Mensforth i985).10In standard deviation of 6 cm (values typicalof those
these studies,shorterbones are consistentlyinterpreted observedin five-year-old-children fromrural
as reflectingincreased stress. This seeminglystraight- Sub-Saharan Africa [Eveleth and Tanner
forwardinterpretation does not take into account that iggo:appendix table 38]); brokencurve,distributionof
thedifferences in statureare observedstrictlyin individ- staturein dead five-year-olds when mortalityis high
uals who died at each age. Alternativeinterpretations (total mortality = 46%); dotted curve,distributionof
are possible when the skeletonsare viewed as nonsurvi- stature among the dead when mortality is low (total
vorswho enteredthe sample as a resultofselectivemor- mortality = 8%). The mean stature of the dead is
talityacting on heterogeneousfrailty. In figure 6, for 95.7 cm under low mortality and 98.6 cm under high
example, we assume that the distributionof stature mortality. At both levels of mortality, the probability
amonglivingchildrenat a givenage is absolutelyinvari- of death is one when statureis less than 8o cm and
ant betweentwo populationsor time spans,thatis, that e-I(x-80) otherwise, wherex is staturein cm and A =
thereis no differential, stress-relatedstunting between O.I2 underlow mortality and 0.04 underhigh
these two groups.We furtherassume that mortalityis mortality.
selectivewith respectto the distributionof stature-in
particular,that shorterchildren are at higherrisk of
death,a relationshipcommonlyobservedin the contem- mortalityand the relationship between stature and
porarydevelopingworld (Kielmann and McCord I978, frailtyare known. Once again,proportionalmortalityis
Chen, Chowdhury,and HuffmanI980, Heywood I982). a poor guide to populationprevalence."
Under these assumptions,variation in the stature of
dead individualsmay indicatedifferent levels ofmortal-
ity (and perhaps stress) but not in the directioncom- ProportionalMortalityand Competing
monlysupposed. When mortalityis high,a largerfrac- Causes of Death
tion of the entiredistributionof statureis represented
amongdead individuals;as a result,dead individualsare One solution to the difficultiesposed above is to aban-
comparativelytall on average(fig.6). If mortalityslack- don any attempt to estimate population prevalences
ens, only the most frail(i.e., short-statured)
individuals fromfrequenciesof skeletal lesions, interpreting such
die. Periodsof low mortalityare therefore characterized frequenciesstrictlyas estimatesofproportionalmortal-
by comparativelylow mean statureamong the dead. In ityor thefractionofdeathsattributableto a givencause.
general,thefrequencyofapparent"stunting"amongthe
dead is uninformativeabout the distributionof stature i i. It is worthnotingthattheinterpretive problemsposedbyselec-
or relativehealth among the living unless the level of tivemortality are not restrictedto comparisonsbetweenancient
samples.In a recentreviewof studieson hard-tissuegrowthand
development, in longbone lengthbetweenprehistoric
differences
io. Differential to life-threatening
susceptibility stresshas also and contemporary samplesare attributedto the "poorerenviron-
been invokedto explainthe smallersize of permanentteethin ments"ofearlierpeoples,thusignoring thefactthattheprehistoric
juvenileswhencomparedwiththeiradultcounterparts(Guagliardo samplesaremadeup ofdeadpeopleandthecontemporary samples
I 9 82). oftheliving(Johnston and Zimmeri989: i8).

This, in effect,is the solution advocated by Cohen shows that proportionalmortalityfromany one cause
(I989:io6), who suggests that "estimates of the inci- is determinedin partby the total numberof causes op-
dence [sic] of disease in skeletal populations are more eratingin the population.Paradoxically,what mightbe
useful for comparison to one another than for direct consideredan improvementin health (eithera reduction
comparisonto ratesreportedin livinggroups."Unfortu- in risk fromcause k or a decrease in the total number
nately, estimates of proportionalmortality"can give of causes) will produce an increase in the proportional
rise to misleadingconclusions if used to compare [the] mortalityfromthe remainingcauses. A familiarexam-
mortalityexperienceof populations with different dis- ple of this phenomenonis the recentincreasein cancer
tributionsof causes of death" (Last I988:I06; see also deaths as a fractionof all deaths in industrialsocieties,
MiettinenI985:260). The reasonforthis is that,by reflectingthe virtual elimination of deaths fromsuch
definition,proportionalmortalityfora single cause of infectiousdiseases as tuberculosis,smallpox,diphtheria,
deathreflectsthe importancenot onlyofthatparticular and typhoid.In thisinstance,the shiftin causes ofdeath
cause but also ofall the othercompetingcauses ofdeath has resultedin greaterlongevitybut also a higherpreva-
experiencedby the population. lence of cancers and more years of life spent disabled,
This factis easiest to demonstrateforcompletelyin- indicatingthat the very concept of "health" may be
dependentcompetingcauses, althoughit is equally true more complex than is oftenassumed.
of interactingcauses. If a population of individuals is The dependenceofproportionalmortalityon the total
exposedto k independentcauses ofdeath,thenthe total distributionof causes would occasion no alarm if we
hazard of death foran individual at age t is simplythe knew everysinglecompetingcause presentin the popu-
sum of the hazards associated with each independent lation. This is difficultenough,and perhapsimpossible,
andJohnson
cause(Elandt-Johnson i98o: 273): to achieve forlivingpopulations.Forprehistoricpopula-
tions, we know only a tiny subset of all competing
htotal(t) = hl(t) + h2(t) + + hk(t) (2) causes, namely, those that leave skeletal traces. As a
result,it becomes extremelydifficultto interpretdiffer-
This is the total hazard experiencedby an individual at ences in proportionalmortalityamongskeletalsamples.
age t, not the totalpopulationhazardcombiningindivid- An increase in the fractionof deaths associated with a
uals ofdiffering frailtyat thatage. The numberofdeaths particularcause may indicate an increased hazard of
to individualsexposedto the totalhazardgivenby equa- death fromthat cause, but it may also indicate a de-
tion 2 depends not only on the total hazard itselfbut crease in the hazard of death fromsome other,totally
also on the numberof individualsexposed to that haz- unrelatedcause. Thus, the same change in proportional
ard (N) and the durationof exposure (8t). For 5t small, mortalitymay signal eitheran improvementor a deteri-
the total number of deaths at age t is approximately orationin the population's health. Once again, we are
Nhtotai(t)*t = Nh1(t)8t + Nh2(t)8t + + Nhk(t)8t. facedwith a fundamentalidentificationproblemwhen
Now suppose that we are interestedspecificallyin dealing with paleopathological and paleodemographic
cause i because it leaves an unambiguousskeletalsigna- data.
ture.The proportionalmortalityattributableto cause i
is simply
PathologicalProcesses and the
Healthiness of the Healed
deathsfromcause i
totaldeaths Paleopathologistsroutinelynote the importanceof dis-
tinguishingactive frominactive or healed lesions, even
while recognizingthatthis simple dichotomizationmay
=
Nh1(t)8t L Nhi(t)8t1
not reflectall the complexitiesof the pathologicalpro-
cess (Mensforthet al. I978, Martin,Goodman,and Arm-
elagos I985, Walker I985, Palkovich i987). As crucial
as this distinctionmay be froma biologicalperspective,
= hl(t) [ hi(t)1= hl(t) hi(t) + hk(t). (3) however, it furthercomplicatesthe interpretation ofpa-
leopathological evidence. The active-inactivedistinc-
tion representsan attemptto separatedisease processes
Writingthe expressionthis way highlightsthe depen- that were ongoing at the time of death, including
dence of the proportionalmortalityassociated with chronicconditions,fromthose thathad occurredearlier.
cause i on the hazard of death fromsome othercause, If this distinctionis correct,the presenceof an inactive
k. lesion indicates survival of a disease process earlierin
If conditionsin our populationchange in such a way life and thus may signifyan individualwhose frailtyis
that the hazard of death fromcause k decreases or is low comparedwith those who died at earlierages.
eliminatedaltogetherwhile the hazard fromcause i is From this perspective,the differing age patternsdis-
unaffected, the proportionalmortalityfromcause i will played by various kinds of lesions take on a new and
then increase even though its hazard remains un- largelyunexploredsignificance.In figure8, we show the
changed.This effectis illustratedin figure7, which also age-specificfrequenciesof cribraorbitalia and porotic

1.0
0.
FIG. 7. Proportionalmortalityfroma specificcause of death (cause i, a disease that leaves a hard-tissue

lesion) as a functionof the total number of competingcauses of death and of the hazard of death fromthe kth
of these causes, assuming that all causes are independentand that the hazard of death fromeach of the first
k - i causes is 0.05.
hyperostosisand ofperiostitisduringthe firstfouryears those with active lesions. In this case, the presenceof a
oflifein the Oneota sample,distinguishing betweenac- healed lesion may actuallybe evidencethatthe individ-
tive and healed lesions. These lesions are of interestbe- ual was of lower frailtyand thereforeat a lower risk of
cause oftheirdistinctetiologies:crudelyspeaking,peri- death; because of his or her superiorcondition,such an
ostitis is a lesion of infectious origin, while cribra individualwas able to survivelong enough to manifest
orbitaliaand porotichyperostosisreflectsynergisticin- a healed lesion. Frailerindividuals,in contrast,would
teractionsof infectionand nutrition.Bearingin mind die soon afterthe onset ofinfection,eitherbeforea bony
that the estimates in figure8 are lesion frequencies responsehad time to develop or duringthe time when
amongthe dead at each age, one mightsuggestthatcri- bone lesions were active. Thus, the presenceofa healed
braorbitaliaand porotichyperostosisrepresentthe com- lesion may sometimesindicatea state of comparatively
mon view of nutritionalstress: children are differen- good overall health.
tiallysusceptibleearlyin life but once stressedremain An alternativeand radicallydifferent interpretation
of
frailthroughoutearlychildhood.Therefore,even skele- the data on cribraorbitalia and porotichyperostosisis
tons with healed lesions are selectively added to the possible. In this interpretation,
virtuallyall individuals
mortalitysample. Periostitis,in contrast,shows a quite developthe lesions earlyin life,but the underlyingcon-
different pattern.Early life is again a time of elevated dition places these individuals at no elevated risk of
stress,but now thereappears to be no differential ten- death whatsoever. Thus, all children survive long
dencyforindividualswithhealed lesions to die and thus enough to recoverand fortheirlesions to heal, unless
enter the skeletal sample. In fact, individuals with theyhappen to die fromsome unrelatedcause. In this
healed lesions appear to be much less likelyto die than scenario,but only in this scenario, the frequenciesof

1.0 1.0
0.8 inactive 7 ?0.8
E |~ -/
/E
E | \active
76 0.6 / 0.6 -
-_
Co Co
0.4 0 0.4
0.2 active 0.2
GL inactive
0.0 0.0 , I Incive
0 1 2 3 4 0 1 2 3 4
Age (years) Age (years)

FIG. 8. Observed proportionsof crania exhibitingcribraorbitalia or porotichyperostosis(left)and skeletons
withperiostitis(right)fromindividuals less than fouryears old in a late prehistoricOneota sample. Skeletons
are classifiedaccordingto whetherthelesions were active or inactive (remodeled)at the time of death.
active and healed lesions in the skeletal sample would Goodman and Armelagos(i988) have reporteddata on
provideunbiased estimatesofthepopulationprevalence enamel hypoplasiain the permanentdentitionforthree
ofsuch lesions. Of course,ifthisprovedto be true,cribra samples of late prehistoricskeletons from Dickson
orbitaliaand porotichyperostosiswould be remarkably Mounds, Illinois.12These data indicate that the overall
uninformativeabout stress and the risk of death. fractionof individuals with such enamel defects in-
Clearly, this interpretationmakes little sense given creasesconsistentlyfromthe earliestto the most recent
what is knownabout the etiologyofthese lesions. How- sample, that the overall mean age at death is lower in
ever,the generalpoint stands: unless we have a strong the most recent sample than in the two earlier ones,
priormodel ofthe way in which a givenlesion, whether and that,except forthe earliest period,skeletonswith
active or inactive, relates to frailtyand of the way in enamel hypoplasia within each sample had a lower
which frailtyvaries among individuals,skeletal lesion mean age at death than their contemporarieswithout
frequenciescannotbe interpreted in any straightforwardenamelhypoplasia.They suggestthreehypothesesto ac-
fashion. count for the lower age at death in individuals with
enamel hypoplasia: (i) that the enamel defectsdirectly
reflectfrailty,lesions and early death being correlated
The Tangled Tales That Dead Folk Tell: An outcomes of an innate constitutionalsusceptibilityto
ExtendedExample stress; (2) that childhood stressresultingin the forma-
tion ofan enamel defectpermanentlydamagedthe indi-
Skeletalsamplesfromarchaeologicalcontextscan be ex- vidual's capacity to mount an effectivebiological re-
pected to presentall the problemsassociated with non- sponse to later stress,and this acquired susceptibility
stationarity,hiddenheterogeneity in risks,and selective
mortalitysimultaneously.In such situations,obvious or
i2. Thisparticular studyis singledoutforfourreasons.First,these
intuitive interpretationsare likely to be badly mis- researchers have been instrumentalin developingthe data-
leading.In this section,we illustratesome of the diffi- recordingprotocolnow commonlyused forhypoplasticenamel
culties that can arise in interpretingthe distributionof defects.Second,theyhave producedsome ofthemostinnovative
hard-tissuelesions that are relics of stressfollowedby osteologicalanalysesto date.Third,theiruse ofcarefully collected
survival.For concreteness,we restrictattentionto the dentaldata,in conjunctionwith skeletal-lesionand age-at-death
information, contributed in theearlyI98os to a reevaluation
ofthe
developmentaldefectof the teethknown as enamel hy- biologicaleffectsof the adoptionof agriculture(Goodmanet al.
poplasia, which provides evidence of stressexperienced I 984). Finally,we believethattheydeservespecialcreditforexplic-
duringchildhood(Goodmanand Rose I990). itlyconsidering in interpreting
multiplehypotheses theirresults.

led to prematuredeathat a latertime; and (3) thatsocial tions: (i) The accumulation of skeletons representsa
conditions produced disproportionateexposure of se- randomsample of deaths froma mixtureof two stable
lected segmentsof the population to stress of diverse populations,'4the advantagedand disadvantagedgroups
origins,membersof social groupswith higherrisks of of our hypothesis;the advantagedgroupinitiallymakes
exposureexhibitingmore stress-relatedenamel defects up io% of the pooled population, but the mix of the
as well as prematuremortality.AlthoughGoodman and two populations changes over time accordingto their
Armelagos (I988) do not rule out any of these three respectivefertility and mortalitypatterns.(2) Bothpopu-
hypothesesand indeed acknowledgethat othersmay be lations experiencefairlyhigh mortality,corresponding
possible,theylean towardthe third. to an expectationof life of about 30 yearsforthe disad-
A fourthhypothesismightalso account fortheirfind- vantagedgroupand 37 yearsforthe advantagedgroup.'5
ings. This hypothesisis based on the fact that enamel (3)The disadvantagedgrouphas low fertility, in particu-
hypoplasiadoes not occur unless the child survivesthe lar a total fertilityrate of four,approximatinglevels re-
periodof stressand resumes normal enamel formation portedforthe !KungSan (Howell I979, Harpendingand
(SucklingI989). Under this hypothesis,the population Wandsnider I982) and the Gainj of highland New
fromwhich each skeletal sample was drawnwas made Guinea (Wood,Johnson,and Campbell I985); the advan-
up oftwo subgroupswith differing levels offertilityand taged population,in contrast,has high fertility,corre-
mortality-one relativelyadvantaged(forwhateverrea- spondingto a total fertility rate of eight(fourand eight
son) and theotherdisadvantaged.Membersofthe advan- are about equally distantfromthe mean total fertility
tagedgroupdid not entirelyescape childhoodinsultbut rateobservedin preindustrialsocieties [Wood I990]). (4)
were able to surviveit long enough to develop enamel Because of theircomparativelypoor condition,children
hypoplasiaand then go on to enjoy higherfertility than in the disadvantagedgroupwho become seriouslyill die
their disadvantaged counterparts.Thus, individuals veryquickly;thus,theydo not surviveepisodes ofstress
with observablelesions were principallyfromthe less that would otherwisehave induced an enamel defect.
frail(i.e., advantaged)group,and theyhad a lowermean For example,the childrenin this groupmightnot have
age at death than the disadvantagedgroup because of sufficientnutritionalreservesto sustain them through
theirhigherfertility, not because ofpoor survival.Ifthe a bout of diarrhealdisease. Consequently,thereare no
differencesin survival and fertilitybetween the two dental signs of stressamong the survivorsof childhood
groupspersistedacross generations,thenthe advantaged in the disadvantagedpopulation simply because those
groupwould come to representan increasingfraction who experience stress do not survive long enough to
of the population as a whole. This hypothesiswould develop hypoplasticenamel defects.In contrast,child-
thereforeexplain the temporaltrendsreportedin both hood illness is oftensurvivedin the advantagedgroup,
lesion frequencyand mean age at death.This hypothesis resultingin numerousolderchildrenand adultswho ex-
and theone preferred byGoodman and Armelagos(i 988) hibitenamel hypoplasiareflecting episodes ofstressear-
are mutuallyexclusive,since underour hypothesisindi- lier in life.
viduals with detectablelesions and earlydeath are pref- Table i lists the characteristicsofthe two model pop-
erentiallydrawnfromthe advantaged group. ulations constructedon the basis of the above assump-
The implicationsofthisfourthhypothesisforthe dis- tions, while figure9 shows how the expected propor-
tributionof skeletons with hard-tissuelesions can be tionsofdead individualswithenamel hypoplasiachange
exploredusing a simple demographicmodel thatgener- over time. The betterhealth of the advantagedpopula-
ates various statistics about hypotheticalpopulations tion is reflectedin its highersurvivaland fertility. As a
giventwo inputparameters,the totalfertility rate (TFR) consequence of its higherfertility, the mean age of the
and the level of mortality.'3Expected proportionsof skeletalremainsfromthe advantagedgroupis I 5 years,
dead individualsdisplayinghypoplasiaat each age were while the mean age of those fromthe disadvantaged
derivedfromthis model under the followingassump- groupis 32. We emphasizethatthisdifference is entirely
attributableto the difference it is uninforma-
in fertility:
tive about any difference in mortality.Finally,because
I3. Underthismodel,age-specificfertility
schedulesweregener- the of a skeletal lesion is indicative of low
atedusingtheratesgivenby Coale and Demeny(i983) fora mean presence
age ofwomenat childbearingequal to 29 years;theserateswere frailty (since frailindividuals die beforedevelopinga le-
multipliedby one-halfthe inputvalue ofthe TFR, roughlyequal
to the grossreproduction rate.Age-specific mortality rateswere
producedby the two-parameter logitmethoddevelopedby Brass I4. A stablepopulationis one withconstantage-specificfertility
(I97I, I975). Using the so-calledAfricanstandardlifetable as a and mortality ratesand an equilibriumage distributionbut not
starting point,a widevarietyofmortality schedulescan be gener- necessarilya zerogrowthrate.The stationarypopulationis a spe-
atedbyvarying eo,theexpectation oflifeat birth(setbytheparam- cial case ofthestablepopulation.
etera. in the Brass model),and the ratioof childhoodto adult I5. The mortality schedulesforthe two populationsare derived
mortality (set by the parameterP). In orderto accommodatethe fromthe Brasslogitmodelusingthe Africanstandardwitha. =
varying waysin whichagesarepooledin publishedpaleopathologi- 0.4 and o.2 in the disadvantagedand advantagedgroups,respec-
cal sources,we havegenerated a smoothyear-by-year survivorship tively,and P = i forbothgroups.Sensitivity testsofthe model
curvebysplineinterpolation throughtheAfricanstandardvalues indicatethatthequalitativeresultsdo notdependuponeitherthe
andhaveused thisas thestandardagainstwhichvariantsurvivor- specificlevels of mortalityor the standardmortalityschedule
shipschedulesare generated. chosen.

TABLE I sion), all the lesions in figure9 are contributedby the

Characteristicsof Two Model Populations advantagedpopulation.In sum, a significanthealth ad-
vantageis reflectedin a lower mean age at death and a
Advantaged Disadvantaged
higherfrequencyofskeletallesions. Betterhealthmakes
Population Population forworse skeletons.
As the intrinsicgrowthrates in table i indicate,our
model does not producea stable mixtureofpopulations:
Inputintomodel the advantagedpopulationis growingrapidlywhile the
Mortality moderate high disadvantagedgroupis almost stationaryand indeed is
(eo = 37 yrs.) (eo = 30 yrs.)
Fertility high low declining slightly.Therefore,given enough time, the
(TFR = 8) (TFR = 4) disadvantagedpopulation will disappearfromthe mix.
Outputfrommodel As a result of this intergenerationalselection process,
Mean age at death I5 32 the mean age at death will go down and the frequency
Mean age at death,individ- 44 53
uals > I5 yrs. ofskeletallesions will go up as timegoes by (fig.9), even
Crudebirthrate(peri,ooo) 56 30 thoughthe characteristicsof the separate populations
Crudedeathrate(peri,ooo) 27 33 remainfixed.The model thus accountsforthe temporal
Intrinsicrate of increase +0.029 -0.003 trends observed at Dickson Mounds (Goodman and
ArmelagosI988).
the Transitionto Agriculture

Reinterpreting
1.0
The issues raised here have serious implications for
_Y
- 160 yrs what is arguablythe most importantpotentialcontribu-
flme
co
c,, tion of paleopathologyand paleodemographyto health
o 0.8 science: elucidation of the biomedical consequences of
the transitionfrom hunting-and-gathering to agricul-
ture. In I982 a decade ofosteologicalfindings pertaining
co
0.6
_ to this transitionwas summarizedand evaluated at the
G) bme- 100 yrs influentialconference"Paleopathologyat the Originsof
Agriculture"(Cohen and ArmelagosI984a). In summa-
ries of this conference,Cohen and Armelagos (i984b)
and Roosevelt(I984) point to a commonbut not univer-
a) 0.4 sal patternin which the adoptionofagricultureand sed-
entarysettlementis associated with a reducedmean age
co\ at death and comparativelyhigh frequenciesof skeletal
0.2
0\
E firre
-50 yr lesions, includingthose attributableto undernutrition
and infectiousdisease. These data are interpretedas in-
0.2 -
dicatingincreasedstressand reducedsurvivalat various
ages, both signs of an apparentdeteriorationin general
Ume- 0 yrs health among the early agriculturalists.Cohen (I989)
summarizesfurtherevidence related to this issue and
0.0 I I I
interpretsit as showingthat agricultureand sedentism
15-24 25-34 35-44 45+ resulted in increased local environmentalcontamina-
tion with pathogens, more frequentperson-to-person
transmissionofinfections,and a decline in dietaryqual-
Age group(years) ityand diversity.
FIG. 9. Age- and period-specific proportionsof While these interpretations may be correct,the data
skeletonswith enamel hypoplasia predictedby a do not forcethemupon us. As is emphasizedby Satten-
mixed-populationmodel with two subpopulations, spiel and Harpending(I983) and by Milner,Humpf,and
one advantaged and the otherdisadvantaged. The Harpending(I989), it is at least as plausible that the
aggregateproportionsofindividuals with enamel shiftin mean age at deathreflectsan increasein fertility
defectswere computed assuming that the advantaged ratherthan an increase in mortalityassociated with a
subpopulationis initially io% of the total aggregate deterioration in generalhealth. Such an elevationin fer-
but that the mixturechanges over time accordingto tility,if it occurred,mighthave reflectedgreateravail-
the intrinsicrates ofincrease listed in table i. The abilityof digestibleweaning foods and, hence, shorter
time span of 150 years is slightlyless than the periods of lactational infecundabilityamong the early
difference in the midpointsof the intervalsused by agriculturalists(see Buikstra, Konigsberg,and Bull-
Goodman and Armelagos (I988) forthe earliest and ingtonI986). Further,the logic developed in this paper
latest Dickson Mounds samples. suggeststhat the higherfrequenciesof skeletal lesions

observedin early agriculturalsamples could reflectan drawnfromwell-documentedmedical collections,and

enhancedabilityto surviveepisodes ofillness and stress the continuedrefinementof field,laboratory,and ana-
or an ameliorationof other,competingand perhapsun- lyticalmethods.'7In contrast,theproblemsdiscussedin
observable causes of death. Thus, the trends summa- thispaperrequirea completerethinkingof the relation-
rizedbyCohenandArmelagos (I984b), Roosevelt(I984), ships among pathological processes, the risk of death,
and Cohen (I989) are equally consistentwith an inter- and the formationof mortalitysamples. In the face of
pretationthat is the opposite of the one theyendorse. demographicnonstationarity,hidden heterogeneityin
It is importantto emphasize thatour reinterpretation frailty,and selective mortality,intuitioncan be a poor
of the health consequences of early agricultureis not guideforevaluatinghow demographicand epidemiolog-
necessarilymore correctthan previous interpretations. ical changesshould be reflectedin a sample ofskeletons.
And, indeed,we suspect that both interpretations may Unfortunately, existingtheorymay be no more useful
be correctfordifferent periodsand locations. The point, as a guidebecause most ofit is concernedwiththe char-
however,is not that we are rightand otherauthorsare acteristicsofthe living,not the dead. As a consequence,
wrong but that the data supportboth interpretations models fordeath distributionsare poorlydeveloped.
equally well. The correctmodel forlinkingdata and in- Whatmust be done to elucidate the complexrelation-
terpretationis in this instance, as in so many others, shipbetweenthe health ofa communityand the charac-
unidentifiable. teristicsof the skeletons it leaves behind? Four tasks
immediatelysuggestthemselves.
First,we need to developdeeperinsightinto thelikely
Is There Hope? sources of heterogeneityin frailtyand the shape of the
frailtydistributionin real populations,work currently
We remain convinced that osteological research will beingpursuedby epidemiologists,physiologists,and ge-
continueto play a centralrole in the studyof human- neticists (Weiss I990). This researchwill need to pay
disease interactions.This is especially trueof attempts due attention to the fact that frailtyis multidimen-
to understandvariation in the health of peoples with sional: differentdisease processes interactwith each
contrastingsubsistenceand settlementsystems,natural otherand also with an individual's constitutionalsus-
environments, levels ofculturalcomplexity,and popula- ceptibilityto stressin determiningfrailty.
tionsizes. Presentcharacterizationsofthe healthofpre- Second, we need to understandhow a given frailty
industrialpopulations are based upon a complicated distributionis related to the distributionof risks of
amalgam of informationfrommodernmedical surveys, death among individuals.A considerablepart of recent
theethnographicand historicalrecords,and archaeologi- demographictheoryhas been devotedto thisissue (Man-
cal excavations of ancient sites (e.g., Cohen I989). Ar- ton and StallardI984, I988; Vaupel I988, 1990), and
chaeologicalevidence is crucial to this effortsince con- we suspect that it may be resolved duringthe coming
temporarypreindustrialpopulations,especiallymodem decade.
hunter-gatherers, are undoubtedlya highlyselect sample Third,we need a betterunderstandingof the details
ofall such populationsthathave ever existed.'6We will ofvariouspathologicalprocesses at the cell, tissue, and
continue to need the perspectiveand time depth that organlevels. Specificaspects of pathologythat need to
archaeologycan provide. be addressedinclude how long it takes to developpartic-
Nevertheless,using the archaeologicalrecordto infer ular hard-tissuelesions, how overall health affectsthe
the health characteristicsof a once-livingpopulationis probabilityof lesion development,and how frailtyand
far more difficultthan is commonly acknowledged. the risk of death vary by stage of lesion development,
Most ofthe widelyrecognizedproblemsassociated with includingthe inactive or healed stage. This is a line of
osteological materials from archaeological sites-in- researchbest pursued by pathologistsworkingwith re-
cludingdeterminingthe age and sex ofskeletons(Buiks- cent,well-documentedbiological materialsand by epi-
tra and Mielke I985, Iscan and Loth I989, Iscan I989, demiologists.'8
St. Hoyme and Iscan I989, Meindl,Russell,and Lovejoy These firstthreetasks are ones to which archaeologi-
I990), the inadequate size and unrepresentative compo- cal osteologistsare unlikelyto make fundamentalcon-
sition of many skeletal samples (Howell I982, Milner, tributions:they must remain consumers ratherthan
Humpf,and HarpendingI989, Paine I989), variableand producersoftherelevanttheoryand observations.There
selective preservationof bones (Gordon and Buikstra is, however,a fourthtask to which all anthropologists
I98I, Waldron I987, Walker, Johnson,and Lambert can contribute,namely,developmentof a betterunder-
I988), and the differential diagnosisof lesion-producing standingof the role played by cultural context in de-
andCook I980, Zim-
I976, Buikstra
diseases(Steinbock
merman and Kelley I982, Ortnerand Putschar I985, I7. Anotherproblem,currently of majorconcernto epidemiolo-
Larsen I987)-can probablybe resolved by additional gistsand demographers butreceivingonlypassingattentionfrom
excavation,the developmentofbetterchronologicaland osteologists, is that of distinguishingprimaryfromcontributory
contextualcontrols,referenceto comparativematerials causes ofdeath(Mantonand StallardI984, Nam i990).
i8. Information on the courseof disease and its relationshipto
mortality in thepreantibiotic erawouldclearlybe ofgreatinterest
i6. See,forexample,thecurrent overthestatusofthe
controversy in this connection,but pertinentdata are difficult to locate and
!Kung(Solwayand Lee I990, Wilmsenand Denbow i990). intepret(Alterand Rileyi989).

terminingheterogeneousfrailtyand the level of selec- birthto age t:

tivemortality.Forexample,interpretation ofthe Oneota
data is facilitatedby the fact that these skeletonswere p(t) = P(o)S1(t)/{p(o)S1(t) + [I - p(o)]S2(t)} (A.2)
drawnfroma relativelysimple tribalsociety.The ceme- = p(?)NW13/(t),
tery,which was completelyexcavated,is comparatively
homogeneousin compositionand appearsto have been
used fora relativelyshortperiod of time, spanningde- where
cades ratherthangenerations.Thereis no archaeological
evidence suggestingthat the sample representsa com- S(t) = p(o)51(t) + [I - p(o)jS2(t) (A.3)
plex accumulationfromdistinctsocial groupswith dif-
ferentialaccess to basic resourcesor exposureto patho- is themean survivalfrombirthto age t in thepopulation
gens, such as might occur in samples drawn from as a whole. Being a constant,p(o) can be writtenas p
complexsocieties or accumulatedovermultiplegenera- with no loss of generality.
tions when eitherfertilityor mortalitywas changing. Combiningequations A.i to A.3 and rearranging, we
While these conditions almost certainlydo not elimi- can write h2(t) as a functionof p, h(t), S(t), hl(t), and
nate the problemofheterogeneousfrailtyentirely,they S1(t):
undoubtedlyminimizeits effects.The Dickson Mounds
skeletal series,in contrast,is more difficultto interpret h2(t) = [E(t)S(t) - ph1(t)S1(t)]/[S(t)
- pS(t)]. (A.4)
because of its cultural context. The cemeteryis large
and its internalorganizationis complex, consistingof Assuming that h(t) is a two-parameternegative Gom-
multiple,superimposedmounds (Harn I980). Much of pertzfunction,then
theburialarea remainsunexcavated,increasingthelike-
lihood that the available sample is selective.The skele- h(t) = ote-t and S(t) = exp [-x(i - e-t)/r]. (A.5)
tons from Dickson Mounds were accumulated over
many generationsspanninghundredsof years duringa If we substitutethese expressionsin equation A.4 and
period of considerable cultural change. Thus, sample provide empirical estimates of oxand p, then h2(t) is
heterogeneity and selectivityare likelyto be ofextreme uniquely determinedby p and hl(t) since Sl(t) can be
importancein theirinterpretation. foundfromhl(t) as
In sum, choosingamong competinginterpretations of
theosteologicalevidencerequirestightcontrolovercul-
tural contextas well as a deeper understandingof the 51(t) = exp -f hl(y)dyl. (A.6)
biologyof frailtyand death. These problemsdeservefar
moreattentionthantheyhave receivedto date ifwe are
to make sense of the biomedical consequences of the Thus, ifwe specifya functionalformforh1(t)and a value
forp, we can immediatelysolve forh2(t).
major social and environmentalchanges that have oc-
curredduringthe course of culturalevolution.
Appendix Comments
Here we present a hazard model of mortalitywith a
two-pointdistributionoffrailty,based on a model origi- MARK N. COHEN
nally developed by Vaupel and Yashin (I985a). We as- Departmentof Anthropology,State Universityof New
sume thatthe populationofinterestcomprisestwo non- York,Plattsburgh,N.Y. 12901, U.S.A. 3I III 92
overlappingfractions,subpopulations i and 2. These
subpopulationsdifferfromeach otherin the level and Wood and colleagues raise a numberof significantques-
age patternof risk of death,but the individualswithin tions about whethercemeterypopulations can be pre-
each subpopulationhave identical risks at each age. If sumed accurately to reflectthe health status of the
hl(t)and h2(t)are the hazardsofdeathat age t in subpop- once-livingpopulations fromwhich they are derived.
ulations i and 2, respectively,then the mean hazard in Specificallythey challenge several of my conclusions
the population as a whole is simply the weightedav- (Cohen and Armelagos I984, Cohen I989) about the
erage, meaning of apparenttrendsin skeletal data related to
the origins of agricultureand the rise of civilization.
h(t) = p(t)hl(t)+ [I - p(t)]h2(t), (A.i) They suggestthat my conclusions are possibly,but not
necessarily,accurate because the skeletal data are ame-
wherep(t) is the fractionof survivingindividualsat age nable to more than one reading.
t who belong to subpopulation i. The value of p(t) is But those conclusions come fromseveral sources of
determinedby the initial mixture of subpopulations data, not just fromskeletons. Skeletal data display an
(i.e., byp(o)) and by Si(t),the probabilitythatan individ- apparentincreasein infectionassociatedwithsedentism
ual in the ith subpopulation (i = i, 2) survivesfrom and large population aggregatesin many parts of the

world.This trendmightbe spurious,as Wood et al. sug- viewed as separate fromrelated demographicconsider-
gest,but it is also predictedby epidemiologicaltheory ations.
and demonstrated, repeatedly,in ethnographiccompari- Paleopathologistsand bioarchaeologistsexcavate and
sons and transitions.Similarly,tuberculosisnot only analyzehuman remainswhich are oftenincompleteand
blossomswithincipienturbanizationin the archaeologi- poorlypreservedand may fall shortof beingrepresenta-
cal recordbut also is clearly a disease of cities in the tive of the population(s)fromwhich they are derived.
modernworld and one which is consideredunlikelyto Even worse,skeletal lesions can be expectedto develop
have been capable ofpropagationin a sparselypopulated only duringperiods of chronicillness, and of those not
preagricultural ancient world. all are known to induce quantifiableor even recogniz-
The apparentincrease in anemia in skeletal popula- able bony changes. This thought-provoking article at-
tionsassociated with farming,sedentism,and largepop- temptsto make explicit,and thereforemore objective,
ulation aggregatesmightalso be spurious,but anemia is the multiple factorswhich play into what the authors
also a well-knownconsequence oftheincreasingparasit- term "selective mortality"and which color all subse-
ism and disease which predictablyaccompanylargerand quent effortsto interpretlesion frequenciesamong sur-
more sedentarygroupsin the modernworld.Moreover, vivors and nonsurvivorsin a particularage-group.The
contemporary hunter-gatherers reallydo have low rates notionof "frailty,"or susceptibilityto stress,presented
of anemia as well as low rates of protein,vitamin,and here is criticalto a deeperunderstandingof both active
mineral deficiency.A similar argumentcan be made and healed lesion frequencies and distributionsand
about the apparentincrease in frequencyof enamel hy- raisesthe largerand morecomplexquestionofjust what
poplasia of teeth associated with the Neolithic revolu- observedskeletal lesion frequenciesreallymean.
tion. Hypoplasia is a general stress markermostlyfor The authors are in good company,because even as
the infantand toddleryears. One prominentcause of early as I985, D. J.Ortner (personal communication)
hypoplasia,weanlingdiarrhea,is, in fact,conspicuously was convinced that the presence of healed skeletal le-
rare or absent among contemporaryhunter-gathererssions suggested that the individual manifestingsuch
even when common in neighboringfarmers.Most diar- bonychangeswas immunologicallycapable of "fighting
rhea in factis density-and sedentism-dependent and is back." As Wood et al. note, "the presenceofan inactive
associated with levels and kinds of malnutritionrarely lesion indicates survival of a disease process earlierin
seen among hunter-gatherers. Moreover,the major epi- life and thus may signifyan individualwhose frailtyis
demic diseases, such as measles, which are also consid- low compared with those who died at earlier ages."
eredpossible causes ofhypoplasiaarguablydid not exist Ratherthan being viewed as the "sick ones," Wood et
in the ancient world. It seems to me that,in the name al. believe that "individualswith detectablelesions and
ofparsimony,the obvious interpretations ofthe skeletal early death are preferentiallydrawn fromthe advan-
trendsin these cases are also the rightones. taged group." That is, the individualswith the healed
On a moregenerallevel,I am concernedwiththe clear bonylesions and the hypoplasticenamel defectsare ac-
pro-stateor procivilizationbias which dominates both tually the healthier ones. I must confess that it has
popularand scientificinterpretations of history(and of takenme a numberofyearsto accept thisargument,but
currentevents). Much of the work that is at stake in I finallyhave; in fact, it makes good inherentsense.
this discussion (Cohen I989) has challenged this bias, What we are looking at when we analyze prehistoric
and it disturbsme that the questions raised by Wood et skeletalpopulationsand observehealed bonypathology
al. emergenow, just as uncivilized life-stylesand the is those who, in a sense, have "made it," to succumb,
meaningof our historyare being reevaluated.In giving perhaps,to a different stressoror groupof stressorslater
the questions raised by Wood et al. the attentionthey in life. This is all the more reason to insist that an ex-
merit,I hope thatwe will rememberto be equally skep- plicitanalyticaldistinctionbe made betweenhealed and
tical of all conclusions from skeletal data (including active lesions; as intuitiveas this may seem, some pa-
those already embedded in our historybooks) and not leopathologicalstudies still do not do it,leavingus with
just discard some of the recent revisions to standard the impossible task of blindlyteasingout the meaning
history. hiddenin the numbers.
While I am convinced that the notion of heteroge-
neous frailtyis an extremelyimportantone, I am consid-
ereablyless optimistic than the authors that we will
LESLIE E. EISENBERG everbe able to develop an index offrailtyforeitherindi-
8S CurtisPlace, Lynbrook,N.Y. 11563, U.S.A. viduals or populations.Fromtheirdiscussion,however,
24 III 92 it is clear thatwe should not assume thathiddenhetero-
geneityis normallydistributedin all populations.It is
In this cautionaryyet optimisticarticle,the authorsad- by applyingthese concepts that we can begin to make
dressa numberofissues fundamentalto the reconstruc- sense of,or at least offercogent competinghypotheses
tion and interpretation ofprehistorichealthusingskele- for explaining,observed bioarchaeologicalphenomena
tal series derived fromarchaeological contexts.While such as the economic,technological,and social changes
my commentsfocus primarilyon the impact of this ar- inherentin the transitionfroma more mobile hunter-
ticle on paleopathological studies, they should not be gathererlife-styleto a more sedentaryagriculturalone.

360 I CURRENT ANTHROPOLOGY Volume 33, Number 4, August-October 1992
That the transitionmay not have been accompaniedby and more general lesions, such as periostitis,could be
a deteriorationin general health status is well worth attributedto otheretiologies. In areas where the trepo-
examiningin lightof the issues raised here. nemal diseases are endemic,such as Africa,morbidityis
highbut mortalityis low. Consequently,the individuals
who exhibitskeletallesions characteristicoftreponema-
DALE L. HUTCHINSON tosis probablyrepresentnot all survivorsof the disease
Departmentof Anthropology,Universityof Illinois, but thosewho have had the disease longest.In this case,
Urbana, Ill. 6I8oI, U.S.A. i9 III 92 periosteal inflammationsmay actually underestimate
the prevalenceof treponematosisin a population. It is
How well a skeletal sample representsthe societyfrom equally as plausible that nonspecificperiostealinflam-
which it is drawnis a long-standingissue. Much of the mations have otheretiologies. This is aside fromother
controversy involvesmethodsforestimatingage and sex health factorswhich might exacerbate the infections,
fromskeletal remains(Bocquet-Appeland Masset i982, such as nutrition.
I985; Buikstraand KonigsbergI985) and biases due to That Wood et al. have leftme thinkingabout other
preservationdifferences(Walker,Johnson,and Lambert examples of hidden heterogeneity,selective mortality,
I988). There is general agreementamong researchers and demographicnonstationarity demonstratesthe util-
that inadequate techniques forestimatingage and sex ityoftheirdiscussion. Considerationof a suite ofpossi-
could result in aberrantdemographicreconstructions. ble explanationsforskeletal lesions is importantforthe
Wood and his colleagues focus on another issue- developmentof more reliable interpretations of disease
inferring the health of a past populationfromfrequen- in past populations.As theypoint out, however,many
cies of pathologypreservedin its skeletal remains. As of the tasks here are likely to fall to researchersother
they point out, many of the problems encounteredin than anthropologists.There is still much to be learned
estimatingthe prevalenceof particulardiseases are the about the interactionof disease, environment,and cul-
same for skeletal and living populations; estimates of tural factorsin the overall epidemiologyof particular
disease prevalencein bothare dependenton the samples diseases. Finally,while anthropologistscan contribute
fromwhich theyare drawn.For example, it is not sur- moretowardan understandingofculturalcontextin the
prisingthatthe prevalenceof tuberculosisin contempo- interpretationof past disease, factorssuch as skeletal
raryU.S. populationsis likely to be greaterin a sample preservationand basic demographicmethodsforskeletal
froma countyhealth clinic subsidized by state funding materialswill still play a role in accurate estimatesof
thanin a sample froma communityhealth-management the health of past populations.
organizationthat is not.
The emphasis on populationsratherthan individuals
in osteological studies duringthe past few decades has RIMANTAS JANKAUSKAS AND GINTAUTAS CESNYS
been an attemptto model studiesofthe dead on studies DepartmentofAnatomy,Histology,and
oftheliving.One questionthatWood et al. raise is when Anthropology, Faculty of Medicine, Vilnius
an aggregateis a population and how many subpopula- University,Ciurlionic 2I/27, 2009 Vilnius,Lithuania.
tionsit contains.This questionwas a majorfocusin the 6 I 92
and Masset(I982, I985) exchanges,
Bocquet-Appel and
their concern with the effectof migrationon demo- This thought-provoking paper is of greatinterestforpa-
graphicreconstructionsremainsa problem. leoanthropologists. While the amount of skeletal mate-
Estimates of disease prevalence in skeletal popula- rial is rapidlyincreasing,most studies of it remainon a
tions are furtherhinderedby the unavailabilityof clini- rathersimpleempiricallevel, limitingthemselvesto the
cal data. Do skeletallesions accuratelyreflectthe preva- merestatementofthe factsobserved.'rhereis a growing
lence of a disease in a living population, or are they need for theoreticalevaluation of these observations,
representativeof the survivorsof a disease who lived and Wood et al.'s paper is a nice attemptto fill this
long enough to manifestthem? The reconstructionof demand. It is axiomatic although often forgottenby
disease prevalencein a past populationfromskeletalle- paleo-osteologiststhat skeletal series firstof all repre-
sions is certainlyproblematic.Many of the lesions present dead people and this means that directextrapola-
servedin skeletal remains are nonspecific.Wood et al. tionfromtheirdata to a livingpopulationis problematic
discuss one such, enamel hypoplasia. Another,perios- (higherfrequenciesof active lesions is one example).
teal inflammation,may resultfrominfectiousdisease or The idea ofhiddenheterogeneity and selectivemortality
fromminor injury.One group of related diseases, the in the dynamicsof death is anotherinterestingand im-
treponematoses,may produce periostealinflammation, portant suggestion. For hunter-gatherer and early ag-
but only some of the individualswho testpositivesero- riculturalsocietiesit is perhapsmorea theoreticalpossi-
logicallyexhibitskeletal involvement(Grin I956, Mur- bility,but forpopulationswith social stratification it is
ray et al. I956). Furthermore,only a small percentage of increasingimportance.The problem can be solved
of the individualswith skeletal lesions develop lesions only throughclose collaboration with archaeologists.
characteristicof treponemalinfection(stellate cranial Anotherquestion of particularinterestis the validityof
lesions, saber tibiae), usually in the secondaryand ter- skeletalmarkersofstress.We completelyagreewiththe
tiarystagesofthe disease. Consequently,the less severe authorsthat therecan be no simple way of interpreting

WOOD ET AL. The Osteological Paradox I 36I
thesemarkers.Forexample,shortstatureand periostitis Recent in-depthstudies of conditions such as enamel

incidence can be understoodbetterwhen the levels of hypoplasia (reviewedby Goodman and Rose I990 and
mortalityare known. In our late-medieval materials, Skinnerand Goodman I992) and porotic hyperostosis
short life-spanis correlatedwith shorterstature,but (Stuart-MacAdam
I985, I987) bringus closerto under-
these samples of shorterstature(and lower level of sex- standingthe implicationsoffindingthese lesions in pre-
ual dimorphism)and shorterlife-spanhave a higherinci- historicpeoples.
dence of healed periosteallesions. Accordingto the hy- A problemnot mentionedin this work is that of dif-
pothesissuggestedby Wood et al., this mightmean that ferentialpreservationof skeletonsbased on age at death
shortstature,shortlife-spanpopulationswith high fre- (see Walker, Johnson,and Lambert I988). This com-
quencies of periosteal lesions (in our case, medieval pounds the problems pointed out by Wood and col-
town populations)were healthier.This conclusion dif- leagues in that it is usually the very young and very
fers dramaticallyfrom traditionalinterpretationsand old who are omittedfromskeletal samples because of
calls forexplanation. differentialpreservation.
This paperis an excellentpresentationofthepossibil- It seems that the best approach we can take at this
of osteologicalmaterialsthatwill
ities of interpretation point is the one these authorssuggest:to providealter-
serveas a basis forfuturediscussionand a call forbetter native explanationsforthe set of data at hand. Along
understandingof culturalcontextas well as of the biol- the same lines as Ortner'splea forbetterdescriptionsof
ogy of pathological processes. It should encourage re- skeletallesions, this approachwill allow othersto work
search collaborationbetween physical and cultural an- with the data and the possible scenarios when future
thropologists. studies provide additional insightsinto the interpreta-
tion of past populations.
M. ANNE KATZENBERG
Departmentof Archaeology,Universityof Calgary, JOHN R. LUKACS
Calgary,Alberta, Canada T2N 1N4. 23 III 92 Departmentof Anthropology,Universityof Oregon,
Eugene,Ore. 97403, U.S.A. 9 iII 92
Wood, Milner, Harpending,and Weiss have very elo-
quentlypointedout that we still have a long way to go In manyways this articleaddressestheoreticaland prac-
beforewe can speak with confidenceabout the health tical concernsforinterpreting thehuman skeletalrecord
of prehistoricpeople. They have also delimited some parallelto those expressedin the earlyI980S bystudents
problems that distort interpretationsof prehistoric of vertebratetaphonomy(Behrensmeyer and Hill I980,
healthfromskeletal remains.While some oftheseprob- Shipman I980). The latterfieldof enquiryis essentially
lems have been broughtforwardin earlierworks (e.g., concernedwith understandingthe demographiccharac-
McHenry I968 on differinginterpretationsof Harris teristicsof livingpopulationsthe betterto interpretthe
lines and Howell i 982 on paleodemographicreconstruc- factorsinfluencingthe creation of vertebratefossil as-
tion), this paper is unique in highlightingand ques- semblages.One wonderswhyit has takenten longyears
tioning specific assumptions in paleodemographyand forphysicalanthropologiststo addresssimilar complex
paleopathologywhich influencelarger-scaleinterpreta- taphonomic processes in human mortuarysamples.
tions of health among earlierpeoples such as those pre- Thoughmanyphysicalanthropologists are familiarwith
sentedin the volume by Cohen and Armelagos(i984a). the worksjust cited,paleopathologyapparentlyhas bor-
My commentsfocus on the problemof evaluatingmor- rowedthese concernsnot directlyfrompaleontologybut
bidity. fromdemography.Nevertheless,the problematicissues
The emphasis on problem-oriented researchin paleo- ofsamplingbias and the complicatingeffectsof distinct
pathology,parallelingresearch in archaeology,has re- demographicpatternson the genesisofvertebratefaunal
sulted in a shiftfromdescribingindividual lesions in asemblagesdirectlyparallel concernsexpressedhere re-
detail to groupinglesions with similar appearancesto- gardingthe measurementand intepretationofpathology
getherand focusingon theirfrequencies.This popula- and vital statisticsin prehistoricskeletal series.
tion approach,startingmost recentlywith the work of Human osteologists and dental anthropologists
Armelagos(I969) and becomingwidespreadthroughout should benefitfromthe cautionarytone of this paper,
the I970S and I980s, has resultedin a wealthoflitera- which serves the valuable purpose of questioning ac-
ture linkingdiet, settlementpatterns,and health (e.g., cepted methods formeasurementand interpretation of
Cohen and Armelagos I984a, Rose and Rathbun I987). health status in prehistoricpopulations. Since the au-
Ortner(i99i) has warnedresearchers ofthedangersof thorsrelyprimarilyupon examplesfromprehistoricNa-
making diagnoses without providingcareful descriptive Americans and many readers may be unfamiliar
tions of bony lesions. He calls fora returnto emphasis with these and similarissues among South Asian popu-
on detailed descriptionsso that the findingsof different lations,my commentwill be devoted to additional ex-
investigatorswill be comparable.While this seems ret- amples fromIndia and Pakistan that generallysupport
rogressive,a more carefulconsiderationof the causes of theircontentions.
lesions would aid in interpretingwhat recoverywith The problemsof hidden heterogeneityin frailtyand
some scar on bone reallymeans in termsof adaptation. sample selectivityare especially well illustratedin In-

dia, wheresocietyis clearlydividedinto distinctgroups: sample, frailin otherrespects.These sex differences

in
the verywealthyand the verypoor. Adequate nutrition, linearenamel hypoplasiaamong BronzeAge Harappans
education, and access to good health care enable the have been interpretedto reflectthe culturally sanc-
wealthy to live a healthier and less stressed life in a tioned differentialtreatment of children commonly
culturally bufferedenvironment.Their impoverished knownas "son preference"or "daughterneglect"(Miller
neighborsare routinelysubjected to malnutrition,lack I985; see also Lukacsand JoshiI992).
of education,more vectors of disease, and minimal or Using naturalratherthan clinical samples,our inves-
inadequatehealth care. This visible heterogeneity in af-
tigationof three living ethnic groups of northwestern
fluenceamong the livingtranslatesinto a culturallyin- India was expectedto show that female Rajputs,mem-
duced variabilityin frailtythat must be consideredsi- bers of a caste groupknown to practice son preference
multaneouslywith the geneticvariationin frailtythat and daughterneglect, displayed a higherincidence of
existswithinboth wealthyand poor segmentsofIndian linearenamel hypoplasiathanmale Rajputs,femaletrib-
society.An individual of "medium frailty"might sur- als, orlow-castefemales(Lukacs and JoshiI992). Gender
vive in a wealthyenvironmentbut perishin a poor one. differences provednot significant,however,and Rajput
Variationsin affluenceand frailtyare not always clearly women had the lowest prevalenceofthe threegroupsof
discerniblein prehistoricmortuarycollections. females studied. These findingssuggestthat the osteo-
AmongtheBronzeAge Harappanstheinterpretive logical paradoxhas its corollaryin studies of the living.
dif-
ficultiesraised by hidden heterogeneityand selectivity In the absence of otherreasonableexplanations,the hy-
are numerousand not easily resolved.Aggregatepreva- pothesis was advanced that if the mortuarysample of
lence rates fordental diseases forthe entireHarappan Rajputfemalescould have been analyzed,a higherpreva-
skeletal sample undoubtedlycombine the prevalences lence of linear enamel hypoplasia would have been
formore than one subpopulationat this 3d-millennium found.
urbansite (Lukacs I992). The series is not largeenough Human osteologistsand dentalanthropologists whose
to permitsubdivisioninto socioeconomic groupson the researchencompasses both livingand prehistoricpopu-
basis offunerary goods or ornatenessofbodyornaments, lations are routinelyconfrontedby the issues raised in
which would be one approachto identifying the preva-this paper, and because of the dramaticdifferencesin
lence of pathologicallesions in subgroupsbased on af- the compositionof theirstudysamples (livingvs. dead)
fluence.Alternatively, thehuman skeletal samplesfrom many of these investigatorsare especially cognizantof
Mesolithic sites of the Gangetic Plains are much more the problemsof hidden heterogeneityin frailtyand se-
likelyto be culturallyhomogeneousthaneithermodern lectivityin skeletal samples. While beingaware ofthese
Indian society or Harappan society and thereforeless problems does not guarantee that workable solutions
susceptibleto these interpretivedilemmas (Lukacs and will be immediatelyforthcoming, it does demand that
HemphillI992, Lukacsand Pal I992). conclusions regardingthe health status of prehistoric
The interpretationof linear enamel hypoplasia data human skeletal series be carefullythoughtout and ad-
on livingIndians and prehistoricHarappansis an excel- vanced with considerablecaution. The authorsof "The
lent example of the complexitiesthat Wood et al. dis- Osteological Paradox" should be commendedforbring-
cuss. At the most elementarylevel, the genderscould ing these problemsto the attentionof a wideraudience.
be consideredas subgroupswhich occur in all human May theirdiscussion generatea higherlevel of achieve-
populations.In the Harappan skeletal sample as whole, ment in paleodemographyand paleopathology!
linear enamel hypoplasia prevalenceis 72.2%, but sig-
nificantdifferences are evidentbetween the sexes both
in this feature(males 52%, females 93%) and in dental JANET W. MCGRATH
caries (Lukacs I992, Hemphill, Lukacs, and Kennedy Departmentof Anthropology,Case WesternReserve
I99I). These results have been interpretedto suggest University,Cleveland, Ohio 44io6-7125, U.S.A.
thatfemaleswere subjectedto greaterstressthan males 2I III 92
duringchildhoodand consumed a more cariogenicdiet
than males as adults. While the mean age of linear "Betterhealth makes for worse skeletons" is a state-
enamel hypoplasia formationis not significantlydif- mentwith complex and interestingimplicationsforthe
ferent for males and females, females are affected study of ancient disease. Wood et al. present a well-
at youngerand older ages and have more events, or reasonedarticlethatpointsto what now seems obvious:
"growthdisruptions,"than males. These observations since skeletallesions developas the resultofa long-term
go beyond mere subgroupprevalence rates to suggest disease process, individuals with skeletal lesions are
that females were ill or malnourishedmore oftenthan likelyto have been ratherhealthy,havingsurvivedlong
males. Among the select sample of Harappan skeletons enoughto develop them.The potentialreinterpretation
available foranalysis,femalesappearto have been more of paleopathologicaldata in light of this discussion is
oftenaffectedby factorscausing linear enamel hypopla- excitingto anticipate.
sia than males and may be consideredfrail,or less well- I confessthat I have always had troubleinterpreting
bufferedagainst those factors,in this respect.Alterna- the data suggestingthat the transitionto agriculturere-
tively,males may be envisionedas less frailwith regard duced health.There is compellingevidencethatthe sed-
to those factorsbut, in that theyare partof a mortuary entism associated with agricultureincreased exposure

to pathogens,therebypotentiallyincreasingthe risk of I99OS, this paperraises a numberof important, far-

death. Many of these pathogens,however,cause acute, reaching points concerning morbidityand mortality
infectiousdisease which would not result in skeletal analyses of prehistoricskeletal populations. In con-
lesions, and thereforethis increase in mortalitywould trastto the aforementionedwork, it adopts a positive
not be reflectedin the skeleton.Discussion has focused approach to the problems it addresses. Responses to
instead on change in diet, and it has always been diffi- Bocquet-Appeland Masset's attackon paleodemography
cult to explain to studentswhy humans turnedto agri- (Buikstraand KonigsbergI985, Van Gerven and Arme-
cultureundersuch conditions.As Wood et al. pointout, lagos I983) constitutedcriticaladvances in a fieldwhich
the work of Armelagos and Goodman has been exem- had been largelysparedself-criticism ifnot externalcri-
plaryherein offering multiplehypothesesto explainthe tiques (cf. Petersen I975, Howell I982). I hope that re-
archeologicalrecord,and they clearly demonstrateyet searchrespondingto the issues raised in this studywill
anotherset of explanations. furthersolidifypaleodemography'sstatus as a valid, al-
The next importantstep,as Wood et al. indicate,will beit specialized subfieldof human demography.
be the clarificationof patternsof frailty.If one aspect I concur with the authors,however,that the points
of frailtyis the immunologic status of the individual, raised here are far more difficultthan those cited by
which is influencedby both diet and infection,then Bocquet-Appeland Masset. While selectivityand demo-
frailty mighthave been affectedby the transitionto agri- graphicnonstationarity are certainlynontrivialmatters,
culture and it could be argued that the transitionin- recentresearchhas addressedthem (cf. Sattenspieland
creased mortalitythroughincreasedfrailty.This, how- HarpendingI983, Saunders and Katzenbergn.d.). In my
ever, leaves unanswered the question why specific opinion, the most bedeviling of the basic conceptual
skeletallesions and skeletalmarkersofstress(e.g.,hypo- problemsraised by the authorsis thatofhiddenhetero-
plasia and Harris lines) are reportedin higherfrequen- geneity.While they effectivelyuse hazards analysis to
cies in populationsin transitionto agriculture.Perhaps defineand describeit, theyalso point to the identifica-
frailerindividuals produce bone lesions more quickly? tionproblemassociated with testingthe goodness-of-fit
We will not know, as Wood et al. point out, until we ofthese models to actual data. As theynote,one way to
understandmore about the way in which frailty,riskof test forgoodness-of-fit is to model frailtydistributions
death,and lesion developmentinteract. on knownbiologicalpatterns,but at the same time they
Althoughtheyaddressdisease in ancient populations detail examples, both contemporary(e.g., diarrhealdis-
only,the question of "hidden heterogeneityof risks" is ease) and prehistoric(e.g., cribraorbitalia,enamel hy-
relevantfor studies of living populations as well. For poplasia), in which counterintuitivemortalitydistri-
example,if the case fatalityrate fora particulardisease butions are either apparent or plausible. Problems of
is equal to the numberdyingof the disease/thenumber interpretation of the resultingill fitbetween such data
with the disease, then differencesin frailtyin the sick and models based on biological patternscan only be
populationwill mean thatnot everyonewiththe disease exacerbatedin prehistoricskeletal analyses, given the
is at equal risk of dying.Differencesin frailtyare not compoundingproblemsof demographicnonstationarity
considered in the calculation of case fatality rates, and/orselectivitybias. To my mind,this is the crucial
mostlybecause ofthe difficulty ofidentifyingthe distri- point where all threeproblemsconverge.
butionoffrailty.Ifwe examine behavioralrisksforpeo- Highlightingthese problemsdoes not mean that pa-
ple who die of this disease, we may erroneouslycon- leodemographyshould be abandoned. Instead,Wood et
clude that a particular behavior or set of behaviors al. are to be congratulatedforbringingthemto theatten-
carriesa higherrisk of mortalitywhen the differences tion of researchers.Considerationof them, while cer-
are reallydue to differences in frailty. tainlydifficult,can only improvepaleodemography.
Wood et al. deserve praise forthe scientificrigorof
theirmultiple-hypothesis approach.In interpreting data
on prehistoricpopulations it is critical to walk a fine DOUGLAS H. UBELAKER
line betweenpat answers that simplyreflectthe biases Departmentof Anthropology, National Museum
of the investigatorsand complete dismissal of the field of Natural History,SmithsonianInstitution,
of research.These authors do this well by reminding Washington,D.C. 20560, U.S.A. II III 92
us of the complexityof the matterwhile retainingen-
thusiasmforthe effortof learningabout health and dis- Wood et al. raise key issues in the interpretation of de-
ease in human populations. mographicand paleopathologicaldata gleaned fromthe
analysisofhuman skeletal remains.One ofthe issues is
relatedto sampling.We have long known thatsampling
ERIC ABELLA ROTH problemsplague our interpretations ofpast human biol-
Departmentof Anthropology, P.O. Box 3050, ogy. If we have no way of knowingfromarcheological
Universityof Victoria,Victoria,B.C., Canada or othersourceswhat inadequacies or complexitiesexist
V8W 3P5. 6 III 92 within the samples used forour studies,then we have
little opportunityto overcome them or to incorporate
In what is inevitablyto become the "Farewell to Pa- theminto a more sophisticatedresearchdesign.I would
leodemography"(Bocquet-Appeland Masset I982) ofthe agreethat selective mortalityand hiddenheterogeneity

are potentialsources of error,but it is importantto re- (oras a responseto stress)are interestingand important.
memberthatsamplingproblemsdo not precludethefor- The well-knownstaturereductionin prehistoricMeso-
mulation of general statementsabout the disease ex- america, or even the unexpected differencesin stature
perience, mortality,and/orfertilityof the population betweenstatusgroupsat Monte Alban,wherethe seem-
represented. inglyhigher-status individualshave shorterstature(Wil-
If interpretedproperly,skeletal lesions usually indi- kinson and Norelli I98I), may be nicely explained by
cate thatthe individualsurviveda disease experienceor differentialmortality,but thereis an opposite relation-
stressepisode,and thatindividualis obviouslyhealthier ship among the prehistoricMaya (Haviland I967) and
than someone who died fromthe same disease experi- at Illinois Hopewell (Buikstra I976). The relationship
ence withoutits havinghad an opportunityto leave its between stature and mortalitycould be investigated
markon the skeleton.As the authorspointout,frequen- withrelativelybountifulhistoricaldata. Staturedata on
cies of skeletal lesions cannot be equated with disease militaryconscriptscould be comparedwith male mor-
frequenciesamongthe living.Similarly,we have learned talityduringthe past 50oyearsin the United States and
that life tables developed frommortalitydata can be an even longerperiodin Europe.
influencedby changes in fertility, migration,and other The bottom line of the pessimistic prognosticators
factorsthatremainlargelyunknownto the investigator. fromPennsylvaniais a seriousone. They note that"pop-
Elucidationof the dynamicrelationshipamong skeletal ulations cannot be comparedmeaningfullyif theirdis-
evidence of disease in mortuarysamples, the distribu- tributionsoffrailtydifferin unknownways." Since het-
tionofages at death,disease frequencyamongthe living erogeneityof frailtyis verylikely and the distribution
representedby the skeletal sample, the demographic offrailtyin prehistoricpopulationsmay be unknowable,
structure,and the health of the living populations re- we are in a pickle. The concept of "identificationprob-
mains a worthwhilebut elusive goal of our research.By lems" is a criticallyimportantone, and this is, as the
raisingissues and clarifyingassumptionsofthe research authorsnote, an area much in need of refinement.We
process,this articlemay enable us to advance. too often accept a skeletal series as a unified entity
ratherthan as a collection of subgroups.Many of our
large,complex skeletal series need to be reinvestigated
RICHARD G. WILKINSON forthe existenceofsuch subdivisions.Subdivisionswith
Departmentof Anthropology,Universityat Albany, geneticbases should be identifiablethroughgross ana-
Albany,N.Y. 12222, U.S.A. io III 92 tomical comparisonsand/ormolecular methods.Subdi-
visions of a more geneticallyhomogeneous population
Wood and colleagues offerpractitionersof paleopopula- which differin their relative frailty,however, would
tion (re)constructionthe provocativepropositionthat seem exceedinglydifficultto identify.The existenceof
"betterhealthmakes forworse skeletons."We are asked a groupofweaning-ageskeletonsmay suggestincreased
to accept the idea thatpeople with lesions-who are,as frailtyrelativeto weanlingdiarrhea,but thissame group
the authors note, indisputably dead-were healthier also provides evidence-by its very existence-of low
thanthosewithoutlesions (who,byvirtueoftheirinclu- frailtyrelative to neonatal and infantmortality.A low
sion in our samples,are equally dead). To the extentthat frequencyof lesions (from,say, porotichyperostosisor
skeletal lesions may representsurvivedstress and the enamel hypoplasia) in this group informsus only that
absence of lesions may denote acute, lethal stress,their membersavoided anemia and growtharrestsearlier.
pointis well taken.As theynote,it has seriousrepercus- In the section "Is There Hope?" we are presented
sions on our interpretations of the health of prehistoric with a litanyof confoundingproblemsand some excel-
populations. lent suggestionsforadvancingour science, specifically
The concept of differentialmorbidity(and mortality), in the area of researchinto questions of the heterogene-
expressedin termsof heterogeneityof frailty,may not ity of frailtyand its relationshipwith distributionsof
be as broadlyapplicable as Wood et al. imply,and the deaths. The call forincreased pathologicalresearchon
concept(s)of health could have been clarified.A lesion- hard-tissuelesions is also well reasoned,but it remains
freeskeleton of 40 yearsat death should not suggestto to be seen whetherspecialists outside of anthropology
us the same thing as a lesion-freeinfantskeleton in and paleopathologycan be coercedinto dealingwith dry
termsof relativehealth,frailty,or immunologicalcom- bone. Finally,we need to understandthe "role played
petence.Aggregatedage-at-deathdata may be interpret- by culturalcontextin determiningheterogeneousfrailty
able as Wood et al. suggest,but the interpretationseems and the level of selective mortality."There are "good"
unlikelyto be applicable to all individuals; some cau- skeletal seriesfromshort-term cemeteries,utilized by a
tionarystatementabout age-specificapplicationis in or- singleculturalunititselfcharacterizedbyrelativeequal-
der,especially since the examples given centeron o-5- ity and, ideally, no migrationto muddy the analytical
yearage-groups.Pathologicalconditionsalso need to be waters.Then there are sites such as Dickson Mounds,
specified,as "betterhealth makes forworse skeletons" representingrelativelylong temporalspans and a good
hardlyapplies to treponemaldiseases, leprosy,and the deal ofculturalcomplexity,bothsynchronically and dia-
like. chronically.We do need to concentrateon the "simple"
The implicationsofthis studyforthe analysisof stat- sitesbeforewe can approachthe issue oftheheterogene-
ure and the use of statureas a measure of adaptability ity of frailtyin the complex ones, but we cannot aban-

WOOD ET AL. The Osteological Paradox I 365
don the latter,which are the rule and not the exception. widespread.Since skeletal lesions are typicallyrareout-
And at some level, these complex sites are more inter- comes and skeletal samples are always small (at least by
esting in that they offertantalizing evidence of bio- epidemiologicalstandards),the probabilityof including
cultural change and of the interrelationshipsamong a lesion in the sample is slim even ifthe associated dis-
populations.It now seems unlikelythat "additional ex- ease was common in the livingpopulation.Third,selec-
cavation" can be pointed to as a potential solution to tivemortalitymay add cases with lesions to the skeletal
data-relatedproblems,and we must continue to make sample at a rate that overrepresents theirprevalencein
advances with the materialat hand. the livingpopulation.This last pointis the one stressed
in ourpaper,in largepartbecause it has notbeen empha-
sized enoughin the existingpaleopathologicalliterature.
We are leftin a quandary.Does the frequencyofskeletal
Reply lesions underestimatedisease prevalenceamongthe liv-
ing because of the sensitivityproblemor overestimate
it because ofthe selectivityand specificityproblems?At
JAMES W. WOOD, GEORGE R. MILNER, HENRY C. this stage,it is anyone's guess. But we can say thiswith
HARPENDING, AND KENNETH M. WEISS confidence:disease prevalence and skeletal-lesionfre-
DepartmentofAnthropology, PennsylvaniaState quency are two very different thingsand, as Ubelaker
University,UniversityPark, Pa. I6802, U.S.A. and Hutchinsonnote, must neverbe equated.
27 Iv 92 One point should be reiteratedforclarity'ssake. The
presence of a particularkind of skeletal lesion is evi-
We thankall the respondentsfortheirthoughtfulcom- dence foreitherpersistenceuntil death ofthe pathologi-
ments. While we cannot pretendthat the problemswe cal processresponsibleforit or survivallong aftera dis-
have flaggedare easy to solve-much less that we have ease episode ended. It is more difficultto interpretthe
solved them-it is encouragingto see how many of our absence of such lesions in ancient skeletons.Their ab-
readersare willing to give them the serious consider- sence may indicate eitherthatthe causal conditionwas
ation they deserve.Most commentatorsrecognizethat not presentor thatearlydeath occurredbeforea distinc-
we are tryingto be constructiveratherthan simplybid- tive skeletal responsehad time to develop. The firstin-
ding farewellto paleodemographyand paleopathology. terpretation is the traditionalexplanation,while the sec-
And most realize that we are urgingconsiderationof ond is the alternativeexploredin our paper. We do not
multiplehypothesesratherthantakingsides on difficult mean to suggestthat the traditionalexplanationmust
and complex issues. Because the comments are gener- always be wrongand the alternativecorrect;the point
ally positive,we confineour response to a few points is that it is generallyimpossible to tell.
thatdeserveamplificationor clarification. Eisenbergsuggeststhat we may be overlyoptimistic
Eisenbergand Hutchinsonpoint out that,in addition about the possibilityof developingan "index of frailty
to the issues we raise,sensitivityis a special concernfor foreitherindividualsor populations." On the contrary,
paleopathology.The sensitivityof a diagnosticcriterion we share her pessimism. Still, we thinkit is worthtry-
(e.g.,presence of a particularkind of skeletal lesion) is ing to measurefrailty,as long as it is acknowledgedjust
the proportionof trulydiseased individualsin a sample how difficulta task it is. We also thinkan alternative
who are identifiedas diseased accordingto that crite- approachis morelikelyto yieldresultsin the shortrun.
rion. As Eisenberg and Hutchinson emphasize, most This approach involves modeling the distributionof
skeletallesions are insensitiveindicatorsoftheirassoci- frailtyin a population,preferably on the basis of sound
ated disease processes in that theytypicallydevelop in biological principlesbut at the veryleast using flexible
only a small fractionof cases (e.g., advanced, chronic statistical distributionsthat will fit a wide varietyof
cases of tuberculosis and treponemal infections).We cases (see Weiss i990). As we detailelsewhere(Wood
agree that sensitivityis a serious problemforpaleopa- et al. i992), such models can then be used to adjust
thologybut did not focus upon it simply because the statisticallyfordiffering frailtydistributionswhen com-
issue has alreadybeen widely discussed in the field.It paringpopulations,even in the absence of individual-
is important,however,to be cautious in respondingto level measuresoffrailty.However,in view ofthe identi-
the sensitivityproblem.For example,ifwe were to find ficationproblem that Roth and Wilkinson so rightly
a few cases of a particularlesion known to have low underscore,it will still be necessary to test as many
sensitivity,we mightbe temptedto inferthat the dis- different specificationsof the frailtydistributionas pos-
ease causing the lesion must have been verywidespread sible.
amongthe living.This inferenceis problematicforthree Lukacs and McGrath make a point of fundamental
reasons. First,as Hutchinson notes, most skeletal le- importance;hiddenheterogeneity and selectivityare not
sions are not onlyinsensitivebut also oflow specificity. justproblemsforosteologicalresearchbut occurin stud-
That is, many distinctpathological conditions induce ies of livingpopulationsas well. McGrath's example of
lesions that are morphologicallysimilar,making accu- the case fatalityrate is especially apt in this regard.We
ratediagnosisdifficultor impossible.Second,absence of would only add that at least a substantialminorityof
a particulartype of lesion in a skeletal sample cannot researchersin demographyand epidemiologyare already
be takenas evidence thatthe associated disease was not strugglingwith these same problems (e.g., Keyfitzand

366 1 CURRENT ANTHROPOLOGY Volume 33, Number 4, August-October 1992
Littman I980, Heckman and Singer I984a, Trussell presenteven when social variationis minimal. None-
and Richards I985, Vaupel and Yashin I985b, Manton theless, Jankauskasand Cesnys are correctin stating
and Stallard I988, Gage i989). There is one important that social complexityonly makes the heterogeneity-
respectin which studiesofthe livinghave an advantage: selectivityproblemworse. In lightof this fact,Wilkin-
when dealingwith livingsubjects,it may be possible to son's advice that we concentrateon the simple sites
"uncover" some of the heterogeneityby actually mea- beforetacklingthe complicatedones is well worthcon-
suringvariablesassociated with frailty.McGrathpoints sidering.
to immunocompetenceas a major componentoffrailty. Several of the commentatorsremindus that it is im-
While immunocompetencecannot be measured on the portant,when consideringthe issues we raise, not to
dead, thereare new proceduresthat allow it to be mea- lose sightof otherproblemsthat have plagued osteolo-
suredon the living,even in remotefieldsettings(Shell gistsformany years.Katzenbergand Hutchinsonpoint
i992). In general,the most satisfying solutionto the hid- to the differentialpreservationof skeletons by age at
den heterogeneity problemis to convertas much of the death,while Jankauskas,Cesnys, and Lukacs highlight
variation as possible fromthe "hidden" to the "mea- the need fordetailed attentionto the culturalcontexts
sured" category.Unfortunately, it is preciselythis ap- fromwhich skeletal samples are drawn.Roth and Ube-
proachthatis so difficult, perhapsimpossible,to imple- laker emphasize the untoward effectsof demographic
mentin archaeologicalstudies.Still,theproblemcannot nonstationarity on paleodemographicanalyses,and Kat-
be solved by ignoringit. zenbergstressesthe need to learnmore about the patho-
Wilkinsonsuggeststhat we place too little emphasis logical processes that result in hard-tissuelesions. We
on the informationprovidedby the age distributionof agree that all these concernsare fundamentallyimpor-
skeletallesions. He is entirelycorrectthatconsideration tant and anticipate that osteologists will continue to
of the age patternof lesion frequenciesis an essential wrestlewith these and other issues that confoundthe
part of any osteological interpretation. We would only interpretation ofancientbones. Such wrestlingis an ab-
pointout thatan examinationof age-specificity was the solute prerequisiteforcontinuedscientificprogress.
veryfoundationof our interpretation of cribraorbitalia, Cohen apparentlyregardsour commentsabout the or-
porotichyperostosis,and periostitisin the Oneota sam- iginsofagricultureas a "challenge" to his own position.
ple. It is equally essential, when tryingto make sense This reactionis disappointing,because we had no wish
of the age distributionof various lesions, to distinguish to become embroiledin the debate-however popular
insofaras possible between hard-tissueresponses that and politically charged-over whetheragricultureand
were active at the time of death and those that were the state were good or bad developmentsin human his-
healed. While recognizingthatit is oftendifficultto dif- tory.As we triedto make clear, the point "is not that
ferentiateactive and inactivelesions when dealingwith we are rightand other authors are wrong" about the
drybone, we concurwith Eisenbergthatit is important effectsof agriculturebut that multiplehypothesesneed
to try.We furthersuggest that well-remodeledskele- to be entertainedand means of distinguishingamong
tal lesions-evidence of events occurringlong before them found. To a large degree, Cohen does precisely
death-are more informativeabout the disease experi- what we advocate. He turns to other kinds of evi-
ence of past peoples than has previouslybeen realized. dence-demographic, biomedical, and epidemiologi-
Using the Oneota skeletons, we show that particular cal-to supplementthe skeletal remains. It is of great
kinds of healed skeletal lesions may indicate groupsof importance,however,that such materialbe used criti-
individualswho experiencedan elevated risk of death cally and with extremecare, since it is subjectto many
relativeto theircontemporaries, while othersmay mark of the same biases and difficultiesof interpretation dis-
individualsof comparativelylow frailty.By examining cussed in our paper, as well as additional confounding
theage patternsofhealed and active lesions and by com- problemsof its own.
paringthose patternsacross lesions of differing etiolo- Cohen points out, forexample, that there are many
gies, we can begin to link pathologicalchanges in bone reports,both archaeologicaland ethnographic, of deteri-
to frailtyin a meaningfulway. For this reason,osteolo- oratinghealth following the settling of formerlyno-
gistsshould neverattemptto drawinferencesfromskel- madic groups.Those reportscannot be dismissedout of
etal lesions consideredindividually. hand,althoughwe note thatthe effectsof sedentismon
Jankauskasand Cesnys make the interestingobserva- morbidityand mortalityin livingpopulationsare more
tion that heterogeneityand selectivityare likely to be- variablethanCohen acknowledges(see, e.g.,Roth I985).
come more importantas social complexityincreases. More fundamental,however,we suggest that two en-
Doubtless they are right,as suggestedin our briefre- tirelydifferent meaningsof the word "health" are being
marks on the archaeological contexts of the Norris confused.One meaning of health is somethingthat ad-
Farms(Oneota) and Dickson Mounds sites. We mustnot verselyaffectsan individual's relativerisk of death. In
take it forgranted,however,thatsimple,small-scaleso- conformitywith what has become standard demo-
cietiesnevercontainsignificantvariationin frailty.One graphicusage, we call this formof health "frailty."A
importantlesson ofthe last 2o yearsofresearchin popu- newbornwho experiencesan unusuallyhighprobability
lation geneticsis that even small, localized, inbredhu- of dyingduringthe firstyear of life is thus "frail."An-
man populationsretaina considerableamountofgenetic othermeaning of health is general physical condition,
variation,some portionof which may have important which if poor might be termed "decrepitude."A thin
phenotypiceffects.Thus, biological variation may be and anemic child with chronicskin lesions and respira-

torydisease is "decrepit."We assume, with Cohen, that By presentingthis example,we do not mean to imply
physicaldecrepitudecan leave signaturesin the skeleton that sedentizationis always accompanied by a decline
and dentition,especially if the illness is survived(e.g., in mortality,forevidencefromotherareas suggeststhat
enamel hypoplasia)or develops into a chroniccondition the opposite sometimes occurs. In general,we consider
(e.g.,skeletal tuberculosis). it extremelyunlikelythatsedentizationalways has sim-
One fundamentalpoint thatwe have triedto make in ple, predictableeffectson mortalityor, forthat matter,
this paper is that these two meanings of health need fertility.In fact,we would go fartherand suggestthat
have no simple relationshipto each other.We suggest in importantrespects
the transitionto settledlifediffers
that in many groups with poor nutritional status- from one location to another. Among the Northern
perhapsincludingmany foragers-childrenare so frail Cree, settlementled to a rapid increase in fertility,
but
that they do not have sufficientreserves to support only because the Canadian governmentsupplied for-
chronicdecrepitude,which takes timeto develop.Infant mula and milk, thus shorteningthe durationof lacta-
and childhood death, when it occurs, happens quickly tional infecundability(Romaniuk 198I). In otherloca-
without leaving any hard-tissuesignature.With more tions,permanentsettlementmay resultin a markedand
food, in contrast, children are capable of sustaining immediate rise in mortality,but only because certain
themselvesin a decrepitstate-a statementthat seems infectiousdiseases such as cholera happen to be epi-
paradoxicalonly if decrepitudeand frailtyare confused. demic in the regionat the time of settlement.Verypos-
If decrepitude lasts long enough before death, then sibly,the developmentof settledagriculturein the Old
markersof this state could show up in the archaeologi- World,especiallywhere domesticatedanimals and non-
cal record.But actual hazardsofdeath,which are propor- human milk were available, had different consequences
itonal to frailty,are lower in such a situation. forfertilityand mortalitythan the parallel process in
Forexample,Harpendingand Wandsnider(i982) have the New World. We will never know unless we reject
described!KungBushmen living in settlementsaround the claim thata uniformresponsealways occurs and its
Ghanzi in Botswana. The children in these settled directionis self-evidentfromexistingdata. In sum, it is
groupswere noticeablydecrepitcomparedwiththeirno- unrealisticto thinkthat the transitionfromforagingto
madic counterpartsin the bush (Truswell and Hansen agriculturemust always have had the same demographic
I976): manywere thinand inactive,and respiratory dis- and biomedical effects.Indeed, we believe that future
ease and skin and eye infectionswere common. Yet the researchshould abandon the conceptof "sedentization"
estimatedinfantmortalityrate in that undeniablyde- as a single process with uniformbiological effectsand
crepitpopulation was half that observed in the bush, concentrateinsteadon the specificmechanismsgovern-
and mortalitybeforeage I5 yearswas one-thirdthat in ing demographyand health in each population.
the bush. The sedentarychildrenwere apparentlymore All the problemswe have raised can be summed up
decrepitbut less frail,despite the factthat theyhad no verysimply: data do not speak forthemselves.This is
betteraccess to effectivemedical care than did nomadic an elementarylesson that has never had the impact it
children.The distinctionbetween frailtyand decrepi- deserves.The informationcontained in empirical data
tude helps explain a paradox firstnoted by Howell can be extractedand interpretedonly when specific
(I979): nomadic !Kung appear to be in good condition models are applied to them.To borrowa wonderfulaph-
buthave mortalityratesat all ages thatare substantially orism fromNathan Keyfitz(I975), "No model, no un-
higherthan those of surroundingsettledgroups. derstanding."In one form or another, everyone uses
Pennington(i992; Penningtonand Harpendingi992), models, even if only vague and nonmathematicalones,
using data reportedby Howell (I979), finds the same when thinkingabout data. All too often,however,these
responseto sedentizationin Ngamiland. Herero pasto- models are implicit and thus unavailable for critical
ralists entered !Kung areas in Ngamiland in the mid- evaluation. It has seemed so obvious that early ages at
I950s, and many !Kung settled at Herero cattleposts, death imply high mortalityor that diseased skeletons
wheremilk and otherfoodswere widely available. The implydiseased populationsthat little thoughthas been
result of settlement,as Penningtonshows, was a drop given to the assumptionsinvolved in these inferences.
in infantmortalityof about 5o%. The largestdecline We have triedto show thateven verysimple alternative
was in the age-intervalI-4 years,correspondingto the models can lead to conclusions that are the exact oppo-
usual age at weaning, when mortalitydroppedto one- site of our immediate intuitions.Of course, as several
fourthits level beforearrival of the Herero. Not only ofour commentatorspoint out, thisproblemofoverem-
were these !Kung newly sedentary,thus meeting the phasis on data at the expenseoftheoryand analysisis by
conditionsof Cohen's model, but they were living in no means restrictedto archaeologicalosteology.Papers
close contact with cattle, a source of zoonoses such as similarto ours could have been writtenfordemography,
tuberculosis.An archaeologicalosteologistofthe future epidemiology,genetics, paleoanthropology,evolution-
mightwell findmuch more skeletal evidenceofdecrepi- aryecology,or any otherfieldof empiricalresearch.But
tude followingsettlementand yet have no way to infer that does not lessen the importanceof the message for
that this increased decripitudewas accompanied by a paleodemographyand paleopathology. The challenge
dramaticdecline in early childhood mortality.This is now is forresearchersto come up with reasonable bio-
particularlytrueifthe age compositionof the sample is logical models that will help us make sense of the way
ignored,as happens all too often in paleopathological skeletal samples are formed and, hence, what they
studies. mean.

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The Osteological Paradox: Problems of Inferring Prehistoric Health from Skeletal Samples

[and Comments and Reply]

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i982. He has been curator oftheMuseumofAnthropology ofthe

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We suggestthatinterpretation of these standardmea- summarystatisticssuch as lifeexpectanciesor themean

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west-centralIllinois (Milnerand Smith i990). A total of Unfortunately,the aggregate-levelhazards of death

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FIG. 4. Numbers of Oneota crania in fiveage-groups 0 5 10 15 20

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tion of the population at risk and the frequencyof le- 100

It is importantto emphasize that this particularre- co

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FIG. 7. Proportionalmortalityfroma specificcause of death (cause i, a disease that leaves a hard-tissue

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TABLE I sion), all the lesions in figure9 are contributedby the

the Transitionto Agriculture

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observedin early agriculturalsamples could reflectan drawnfromwell-documentedmedical collections,and

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terminingheterogeneousfrailtyand the level of selec- birthto age t:

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thesemarkers.Forexample,shortstatureand periostitis Recent in-depthstudies of conditions such as enamel

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dia, wheresocietyis clearlydividedinto distinctgroups: sample, frailin otherrespects.These sex differences

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to pathogens,therebypotentiallyincreasingthe risk of I99OS, this paperraises a numberof important, far-

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ReferencesCited . I984. "Subsistenceand healthin thelowerIllinoisVal-

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